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Genetics Major for College: Exploring DNA and RNA

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When we think of DNA, most of us picture a long and twisting double helix. But beyond its iconic structure lies a world of scientific secrets waiting to be unlocked. And what about RNA? "Never heard of it, Hulio." Its stands for ribonucleic acid, another key player in the game of life. Inspire future scientists by introducing them to a major in Genetics. Catch their interest with our editable template and offer a brief preview into this field of study. Our design contains gradients and thematic illustrations, besides text boxes, infographics, tables, graphs and more.

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Genetic Alliance; The New York-Mid-Atlantic Consortium for Genetic and Newborn Screening Services. Understanding Genetics: A New York, Mid-Atlantic Guide for Patients and Health Professionals. Washington (DC): Genetic Alliance; 2009 Jul 8.

Understanding Genetics: A New York, Mid-Atlantic Guide for Patients and Health Professionals.

Chapter 1 genetics 101.

Almost every human trait and disease has a genetic component, whether inherited or influenced by behavioral factors such as exercise. Genetic components can also modify the body’s response to environmental factors such as toxins. Understanding the underlying concepts of human genetics and the role of genes, behavior, and the environment is important for appropriately collecting and applying genetic and genomic information and technologies during clinical care. It is important in improving disease diagnosis and treatment as well. This chapter provides fundamental information about basic genetics concepts, including cell structure, the molecular and biochemical basis of disease, major types of genetic disease, laws of inheritance, and the impact of genetic variation.

• 1.1 Cells, Genomes, DNA, and Genes

Cells are the fundamental structural and functional units of every known living organism. Instructions needed to direct activities are contained within a DNA (deoxyribonucleic acid) sequence. DNA from all organisms is made up of the same chemical units (bases) called adenine, thymine, guanine, and cytosine, abbreviated as A, T, G, and C. In complementary DNA strands, A matches with T, and C with G, to form base pairs. The human genome (total composition of genetic material within a cell) is packaged into larger units known as chromosomes—physically separate molecules that range in length from about 50 to 250 million base pairs. Human cells contain two sets of chromosomes, one set inherited from each parent. Each cell normally contains 23 pairs of chromosomes, which consist of 22 autosomes (numbered 1 through 22) and one pair of sex chromosomes (XX or XY). However, sperm and ova normally contain half as much genetic material: only one copy of each chromosome.

Each chromosome contains many genes, the basic physical and functional units of heredity. Genes are specific sequences of bases that encode instructions for how to make proteins. The DNA sequence is the particular side-by-side arrangement of bases along the DNA strand (e.g., ATTCCGGA). Each gene has a unique DNA sequence. Genes comprise only about 29 percent of the human genome; the remainder consists of non-coding regions, whose functions may include providing chromosomal structural integrity and regulating where, when, and in what quantity proteins are made. The human genome is estimated to contain 20,000 to 25,000 genes.

Although each cell contains a full complement of DNA, cells use genes selectively. For example, the genes active in a liver cell differ from the genes active in a brain cell because each cell performs different functions and, therefore, requires different proteins. Different genes can also be activated during development or in response to environmental stimuli such as an infection or stress.

• 1.2 Types of Genetic Disease

Many, if not most, diseases are caused or influenced by genetics. Genes, through the proteins they encode, determine how efficiently foods and chemicals are metabolized, how effectively toxins are detoxified, and how vigorously infections are targeted. Genetic diseases can be categorized into three major groups: single-gene, chromosomal, and multifactorial.

Changes in the DNA sequence of single genes, also known as mutations, cause thousands of diseases. A gene can mutate in many ways, resulting in an altered protein product that is unable to perform its normal function. The most common gene mutation involves a change or “misspelling” in a single base in the DNA. Other mutations include the loss (deletion) or gain (duplication or insertion) of a single or multiple base(s). The altered protein product may still retain some normal function, but at a reduced capacity. In other cases, the protein may be totally disabled by the mutation or gain an entirely new, but damaging, function. The outcome of a particular mutation depends not only on how it alters a protein’s function, but also on how vital that particular protein is to survival. Other mutations, called polymorphisms, are natural variations in DNA sequence that have no adverse effects and are simply differences among individuals.

In addition to mutations in single genes, genetic diseases can be caused by larger mutations in chromosomes. Chromosomal abnormalities may result from either the total number of chromosomes differing from the usual amount or the physical structure of a chromosome differing from the usual structure. The most common type of chromosomal abnormality is known as aneuploidy, an abnormal number of chromosomes due to an extra or missing chromosome. A usual karyotype (complete chromosome set) contains 46 chromosomes including an XX (female) or an XY (male) sex chromosome pair. Structural chromosomal abnormalities include deletions, duplications, insertions, inversions, or translocations of a chromosome segment. (See Appendix F for more information about chromosomal abnormalities.)

Multifactorial diseases are caused by a complex combination of genetic, behavioral, and environmental factors. Examples of these conditions include spina bifida, diabetes, and heart disease. Although multifactorial diseases can recur in families, some mutations such as cancer can be acquired throughout an individual’s lifetime. All genes work in the context of environment and behavior. Alterations in behavior or the environment such as diet, exercise, exposure to toxic agents, or medications can all influence genetic traits.

• 1.3 Laws of Inheritance

The basic laws of inheritance are useful in understanding patterns of disease transmission. Single-gene diseases are usually inherited in one of several patterns, depending on the location of the gene (e.g., chromosomes 1-22 or X and Y) and whether one or two normal copies of the gene are needed for normal protein activity. Five basic modes of inheritance for single-gene diseases exist: autosomal dominant, autosomal recessive, X-linked dominant, X-linked recessive, and mitochondria. (See diagram on following page.)

• 1.4 Genetic Variation

All individuals are 99.9 percent the same genetically. The differences in the sequence of DNA among individuals, or genetic variation, explain some of the differences among people such as physical traits and higher or lower risk for certain diseases. Mutations and polymorphisms are forms of genetic variation. While mutations are generally associated with disease and are relatively rare, polymorphisms are more frequent and their clinical significance is not as straightforward. Single nucleotide polymorphisms (SNPs, pronounced “snips”) are DNA sequence variations that occur when a single nucleotide is altered. SNPs occur every 100 to 300 bases along the 3 billion-base human genome. A single individual may carry millions of SNPs.

Although some genetic variations may cause or modify disease risk, other changes may result in no increased risk or a neutral presentation. For example, genetic variants in a single gene account for the different blood types: A, B, AB, and O. Understanding the clinical significance of genetic variation is a complicated process because of our limited knowledge of which genes are involved in a disease or condition and the multiple gene-gene and gene-behavior-environment interactions likely to be involved in complex, chronic diseases. New technologies are enabling faster and more accurate detection of genetic variants in hundreds or thousands of genes in a single process.

• Selected References

Department of Energy, Human Genome Project Education Resources www.ornl.gov/sci/techresources/Human_Genome/education/education.shtml

Genetics Home Reference http://www.ghr.nlm.nih.gov

National Human Genome Research Institute www.genome.gov/health

Online Mendelian Inheritance in Man www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=omim

All Genetic Alliance content, except where otherwise noted, is licensed under a Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

• Cite this Page Genetic Alliance; The New York-Mid-Atlantic Consortium for Genetic and Newborn Screening Services. Understanding Genetics: A New York, Mid-Atlantic Guide for Patients and Health Professionals. Washington (DC): Genetic Alliance; 2009 Jul 8. CHAPTER 1, GENETICS 101.
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Genetics PPT

Genetics is a interesting field of biology that explores the mechanisms and processes of inheritance, variation, and evolution in living organisms. From identifying the genetic basis of diseases to developing genetically modified crops, genetics has significant applications in various areas of science, medicine, and agriculture. Here you can find easy Genetics Power Point Presentation to study the principles and concepts of genetics and molecular genetics. You can download all Genetics PPT absoutely free without any subscription or payments.

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Introduction to Genetics

Jul 27, 2014

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Introduction to Genetics. Chapter 11. What we already know…. In sexual reproduction, gametes (sperm and egg) unite to form the first diploid cell (zygote)……. Back in Meiosis I……. During Anaphase I, homologous chromosomes separated……

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Presentation Transcript

Introduction to Genetics Chapter 11

What we already know… • In sexual reproduction, gametes (sperm and egg) unite to form the first diploid cell (zygote)……

Back in Meiosis I…… • During Anaphase I, homologous chromosomes separated…… • Law of Independent Assortment - chromosomes assort independently, not individual genes

The Work of Gregor Mendel Section 11.1 Mendel's Pea Plants (start at 10 min)

The Father of Heredity The modern science of genetics was founded by an Austrian monk named Gregor Mendel. Mendel was in charge of the monastery garden, where he was able to do the work that changed biology forever.

The Experiments of Gregor Mendel Mendel carried out his work with ordinary garden peas, partly because peas are small and easy to grow. A single pea plant can produce hundreds of offspring. Today we call peas a “model system.”

The Experiments of Gregor Mendel By using peas, Mendel was able to carry out, in just one or two growing seasons, experiments that would have been impossible to do with humans and that would have taken decades—if not centuries—to do with other large animals.

Vocabulary: • Genotype • Phenotype • Dominant • Recessive • Homozygous • Heterozygous • Heredity • Genetics • Fertilization • Self-Pollination • Cross-Pollination • Traits • Alleles

The Experiments of Gregor Mendel • Every living thing—plant or animal, microbe or human being—has a set of characteristics inherited from its parent or parents. • The delivery of characteristics from parent to offspring is called heredity. • The scientific study of heredity, known as genetics, is the key to understanding what makes each organism unique. Mendelian Heredity 1 Teacher Tube (stop at 5:30)

The Role of Fertilization • Mendel knew that the male part of each flower makes pollen, which contains sperm—the plant’s male reproductive cells. • Similarly, Mendel knew that the female portion of each flower produces reproductive cells called eggs.

Pollination: • Occurs when pollen grains produced in the male reproductive parts of a flower, called the anthers, are transferred to the female reproductive parts of a flower called the stigma.

The Role of Fertilization • During sexual reproduction, male and female reproductive cells join to produce a new cellin a process known as fertilization. In peas, this new cell develops into a tiny embryo encased within a seed. • Pea flowers are normally self-pollinating, which means that sperm cells fertilize egg cells from within the same flower. • A plant grown from a seed produced by self-pollination inherits all of its characteristics from the single plant that bore it. • In effect, it has a single parent.

The Role of Fertilization • Mendel’s garden had several stocks of pea plants that were “true-breeding,” meaning that they were self-pollinating, and would produce offspring with identical traits to themselves. In other words, the traits of each successive generation would be the same. • A traitis aspecific characteristic of an individual, such as seed color or plant height, and may vary from one individual to another.

The Role of Fertilization • Mendel decided to “cross” his stocks of true-breeding plants—he caused one plant to reproduce with another plant. • To do this, he had to prevent self-pollination. He did so by cutting away the pollen-bearing male parts of a flower and then dusting the pollen from a different plant onto the female part of that flower, as shown in the figure.

The Role of Fertilization • This process, known as cross-pollination, produces a plant that has two different parents. • Cross-pollination allowed Mendel to breed plants with traits different from those of their parents and then study the results.

The Role of Fertilization • Mendel studied seven different traits of pea plants, each of which had two contrasting characteristics. Mendel crossed plants with each of the seven contrasting characteristics and then studied their offspring. • The offspring of crosses between parents with different traits are called hybrids.

Genes and Alleles Each of the traits Mendel studied was controlled by one gene that occurred in two contrasting varieties. These gene variations produced different expressions, or forms, of each trait. The different forms of a geneare called alleles.

Genotype: • Genetic make-up of an organism • Examples: Aa, BB, cc

Phenotype: • Physical characteristics of an organism • Examples: blue eyes, brown hair, freckles

Dominant: • Form of a gene that is expressed even if present with a contrasting recessive allele. • Example: Aa A = dominant allele

Recessive: • Form of a gene (allele) that is only expressed in the homozygous state. • Example: bb

Homozygous (Purebred): • Organism that has two identical alleles for a particular trait. • Examples: AA, bb, CC, dd

Heterozygous (Hybrid): • Organism that has two different alleles for the same gene. • Examples: Aa, Bb, Cc, Dd

Genes and Alleles When doing genetic crosses, we call the original pair of plants the P generation, or the parentalgeneration.

Genes and Alleles • Their offspring are called the F1, or “first filial,” generation. The offspring of a cross between two F1 individuals are called the F2, or “second filial” generation.

Genes and Alleles • For each trait studied in Mendel’s experiments, all the offspring had the characteristics of only one of their parents, as shown in the table.

Genes and Alleles • In each cross, the nature of the other parent, with regard to each trait, seemed to have disappeared.

Genes and Alleles • From these results, Mendel drew two conclusions. His first conclusion formed the basis of our current understanding of inheritance. • An individual’s characteristics are determined by factors that are passed from one parental generation to the next. • Scientists call the factors that are passed from parent to offspring genes.

Dominant and Recessive Traits • Mendel’s second conclusionis called the Principle of Dominance. This principle states that some alleles are dominant and others are recessive. • An organism with at least one dominant allele for a particular form of a trait will exhibit that form of the trait. • An organism with a recessive allele for a particular form of a trait will exhibit that form only when the dominant allele for the trait is not present.

Dominant and Recessive Traits • In Mendel’s experiments, the allele for tall plants was dominant and the allele for short plants was recessive. Likewise, the allele for yellow seeds was dominant over the recessive allele for green seeds

Segregation: During gamete formation, the alleles for each gene segregate from each other, so that each gamete carries only one allele for each gene.

Segregation • Mendel wanted to find out what had happened to the recessive alleles. • To find out, Mendel allowed all seven kinds of F1 hybrids to self-pollinate. The offspring of an F1 cross are called the F2 generation. • The F2 offspring of Mendel’s experiment are shown.

The F1 Cross • When Mendel compared the F2 plants, he discovered the traits controlled by the recessive alleles reappeared in the second generation. • Roughly one fourth of the F2 plants showed the trait controlled by the recessive allele.

Explaining the F1 Cross • Mendel assumed that a dominant allele had masked the corresponding recessive allele in the F1 generation. • The reappearance of the recessive trait in the F2 generation indicated that, at some point, the allele for shortness had separated from the allele for tallness.

Explaining the F1 Cross • How did this separation, or segregation, of alleles occur? • Mendel suggested that the alleles for tallness and shortness in the F1 plants must have segregated from each other during the formation of the sex cells, or gametes.

The Formation of Gametes • Let’s assume that each F1 plant—all of which were tall—inherited an allele for tallness from its tall parent and an allele for shortness from its short parent (Tt).

The Formation of Gametes • When each parent, or F1 adult, produces gametes, the alleles for each gene segregate from one another, so that each gamete carries only one allele for each gene.

Independent Assortment • How do alleles segregate when more than one gene is involved? • The principle of independent assortment states that genes for different traits can segregate independently during the formation of gametes. 100 Greatest Discoveries (Genetics) 45 min – stop at 8 for Mendel

Applying Mendel’s Principles Section 11.2

THINK ABOUT IT • Nothing in life is certain. • If a parent carries two different alleles for a certain gene, we can’t be sure which of those alleles will be inherited by one of the parent’s offspring. • However, even if we can’t predict the exact future, we can do something almost as useful—we can figure out the odds.

Probability and Punnett Squares • Mendel realized that the principles of probability could be used to explain the results of his genetic crosses. Probability is the likelihood that a particular event will occur. • Probability = ________________________________________ Number of favorable outcomes (ways it can happen) Number of possible outcomes

Probability and Punnett Squares • For example, there are two possible outcomes of a coin flip: The coin may land either heads up or tails up. • The chance, or probability, of either outcome is equal. Therefore, the probability that a single coin flip will land heads up is 1 chance in 2. • This amounts to 1/2, or 50 percent.

Probability and Punnett Squares Example: the chances of rolling a "4" with a die • Number of ways it can happen: 1 (there is only 1 face with a "4" on it) • Total number of outcomes: 6 (there are 6 faces altogether)

Probability and Punnett Squares • If you flip a coin three times in a row, what is the probability that it will land heads up every time? • Each coin flip is an independent event, with a one chance in two probability of landing heads up. • Therefore, the probability of flipping three heads in a row is: ½x ½ x ½ = 1/8

Probability and Punnett Squares • As you can see, you have 1 chance in 8 of flipping heads three times in a row. • Past outcomes do not affect future ones. Just because you’ve flipped 3 heads in a row does not mean that you’re more likely to have a coin land tails up on the next flip.

Using Segregation to Predict Outcomes The way in which alleles segregate during gamete formation is every bit as random as a coin flip. Therefore, the principles of probability can be used to predict the outcomes of genetic crosses. Probability is always between 0 and 1

Using Punnett Squares One of the best ways to predict the outcome of a genetic cross is by drawing a simple diagram known as a Punnett square. Punnett squares allow you to predict the genotype and phenotype combinations in genetic crosses using mathematical probability.

How To Make a Punnett Square for a One-Factor (MONOHYBRID) Cross Write the genotypes of the two organisms that will serve as parents in a cross. In this example we will cross a male and female osprey that are heterozygous for large beaks. They each have genotypes of Bb. Example: Bb and Bb

How To Make a Punnett Square Determine what alleles would be found in all of the possible gametes that each parent could produce. Bb B b

How To Make a Punnett Square Draw a table with enough spaces for each pair of gametes from each parent. Enter the genotypes of the gametes produced by both parents on the top and left sides of the table.

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Who discovered the structure of DNA?

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• National Center for Biotechnology Information - The Structure and Function of DNA
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What does DNA do?

Deoxyribonucleic acid (DNA) is an organic chemical that contains genetic information and instructions for protein synthesis . It is found in most cells of every organism. DNA is a key part of reproduction in which genetic heredity occurs through the passing down of DNA from parent or parents to offspring.

What is DNA made of?

DNA is made of nucleotides . A nucleotide has two components: a backbone, made from the sugar deoxyribose and phosphate groups, and nitrogenous bases, known as cytosine , thymine , adenine , and guanine . Genetic code is formed through different arrangements of the bases.

The discovery of DNA’s double-helix structure is credited to the researchers James Watson and Francis Crick , who, with fellow researcher Maurice Wilkins , received a Nobel Prize in 1962 for their work. Many believe that Rosalind Franklin should also be given credit, since she made the revolutionary photo of DNA’s double-helix structure, which was used as evidence without her permission.

Can you edit DNA?

Gene editing today is mostly done through a technique called Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR), adopted from a bacterial mechanism that can cut out specific sections in DNA. One use of CRISPR is the creation of genetically modified organism (GMO) crops.

What’s the difference between DNA and RNA?

DNA is the master blueprint for life and constitutes the genetic material in all free-living organisms. RNA uses DNA to code for the structure of proteins synthesized in cells . Learn more about the differences between DNA and RNA.

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DNA , organic chemical of complex molecular structure that is found in all prokaryotic and eukaryotic cells and in many viruses . DNA codes genetic information for the transmission of inherited traits.

A brief treatment of DNA follows. For full treatment, see genetics: DNA and the genetic code .

The chemical DNA was first discovered in 1869, but its role in genetic inheritance was not demonstrated until 1943. In 1953 James Watson and Francis Crick , aided by the work of biophysicists Rosalind Franklin and Maurice Wilkins , determined that the structure of DNA is a double-helix polymer , a spiral consisting of two DNA strands wound around each other. The breakthrough led to significant advances in scientists’ understanding of DNA replication and hereditary control of cellular activities.

Each strand of a DNA molecule is composed of a long chain of monomer nucleotides . The nucleotides of DNA consist of a deoxyribose sugar molecule to which is attached a phosphate group and one of four nitrogenous bases : two purines ( adenine and guanine ) and two pyrimidines ( cytosine and thymine ). The nucleotides are joined together by covalent bonds between the phosphate of one nucleotide and the sugar of the next, forming a phosphate-sugar backbone from which the nitrogenous bases protrude. One strand is held to another by hydrogen bonds between the bases; the sequencing of this bonding is specific—i.e., adenine bonds only with thymine, and cytosine only with guanine.

The configuration of the DNA molecule is highly stable, allowing it to act as a template for the replication of new DNA molecules, as well as for the production ( transcription ) of the related RNA (ribonucleic acid) molecule. A segment of DNA that codes for the cell’s synthesis of a specific protein is called a gene .

DNA replicates by separating into two single strands, each of which serves as a template for a new strand. The new strands are copied by the same principle of hydrogen-bond pairing between bases that exists in the double helix. Two new double-stranded molecules of DNA are produced, each containing one of the original strands and one new strand. This “semiconservative” replication is the key to the stable inheritance of genetic traits.

Within a cell, DNA is organized into dense protein-DNA complexes called chromosomes . In eukaryotes , the chromosomes are located in the nucleus , although DNA also is found in mitochondria and chloroplasts . In prokaryotes , which do not have a membrane-bound nucleus, the DNA is found as a single circular chromosome in the cytoplasm . Some prokaryotes, such as bacteria , and a few eukaryotes have extrachromosomal DNA known as plasmids , which are autonomous , self-replicating genetic material. Plasmids have been used extensively in recombinant DNA technology to study gene expression.

The genetic material of viruses may be single- or double-stranded DNA or RNA. Retroviruses carry their genetic material as single-stranded RNA and produce the enzyme reverse transcriptase , which can generate DNA from the RNA strand. Four-stranded DNA complexes known as G-quadruplexes have been observed in guanine-rich areas of the human genome .

Welcome to the Bedinger Lab

Topics in Advanced Genetics

(example from fall 2012).

This course is designed to follow an introductory course in genetics and molecular biology (BZ350, LS201 or SC330), for advanced undergraduates or beginning graduate students wishing to pursue advanced topics in genetics. Gene systems in diverse model organisms will be covered, including those of prokaryotes, fungi, plants and animals. The course is not intended to be comprehensive– rather, a number of topics will be covered in some depth. Reading materials for this course will be made available electronically on RamCT. We will also be using material from textbooks that are available on line. We will note which textbook a figure is taken from, you can access the relevant portion at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books One goal of this course is to demonstrate the range of biological problems that can be addressed using classical and molecular genetics. Another goal is to have students critically evaluate and present a scientific paper from a leading journal on a topic in genetics. Grades will be based on a total of 500 points. In Dr. Bedinger’s half of the course, one 10 point pre-quiz, three problem sets (10 points each), and two 80 point exams will be given. Dr. Garrity’s half will involve four problem sets (10 pts each) and two 80 point exams. In-class activities will be worth 20 points. Students will also make a PowerPoint presentation of a recent journal paper, worth 80 points.

COURSE TOPICS

• Molecular techniques: Analyzing DNA (including genomes), RNA and proteins
• Genetic techniques: Identifying and analyzing mutants, forward and reverse genetics
• Bacteria, not as simple as you think
• Advantages of prokaryotic systems
• Chemotaxis, a simple signal transduction pathway
• Saccharomyces cerevisiae (budding yeast), a unicellular eukaryote
• Gene replacement and artificial chromosomes
• Dissection of the cell cycle
• Arabidopsis thaliana, a plant model
• Plant strategies in development
• How does an organ know what it is? Floral organ development
• Development and disease: using genetics to dissect developmental processes
• Caenorhabditis elegans, a simple multicellular organism
• Building a genetic pathway: vulva development
• Drosophila melanogaster, genetic tools extraordinaire
• Genes that interact: eye development
• Zebrafish (Danio rerio), new insights into vertebrate development
• Is organogenesis modular?
• Mouse, models for human disease
• The power of targeted mutagenesis: Hox genes and body plan
• Stem cells, the potential and the problems, Cancer and genetics
• Introduction to model organisms
• Analyzing DNA and cloning
• Analyzing gene expression – RNA
• Microarrays, Review quiz on genetics and molecular biology
• Analyzing gene expression – Proteins [Problem set #1 due]
• Forward genetics: mutagenesis and analyzing mutants
• Making transgenic organisms
• Reverse genetics [Problem set #2 due]
• EXAM 1 – molecular and genetic techniques
• Bacteria as a genetic system
• Bacterial chemotaxis I
• Bacterial chemotaxis II
• Yeast as a genetic system
• Genetics of the cell cycle I
• Genetics of the cell cycle II
• Arabidopsis, a model for plant developmental genetics
•  Floral organ formation I [Problem set #3 due]
• Floral organ formation II
• C elegans : a simple multicellular organis
• Identifying essential genes
• Vulva development: Ordering genes into a pathway
• Drosophila: genetics extraordinaire [Problem set #4 due]
• Genetic mosaics
•  Eye development: suppressor and enhancer screens
• Genomics: the Drosophila genome project [Problem set #5 due]
•   EXAM 3 [Selection of scientific paper approved by this date]
• Zebrafish: new insights into vertebrate development
• Approaches to genetic screens in vertebrates
• The genetic basis of organogenesis I
• The genetic basis of organogenesis II
•  Mouse as a premier vertebrate model [Problem set #6 due]
•  Using transgenic tools [talk outline and reference list due]
•  Mouse body plan – revelations of Hox gene mutants
•  Mouse models of human disease
•  Stem cells [Problem set #7 due]
•  Regenerative medicine – recent advances
•  Special topics

Last 4 class periods- Student Presentations

1. Review quiz (10 points): A list of genetic and molecular biology terms and basic problems from introductory genetics will be presented the first day of class. An in-class quiz on this material will be conducted on September 3, based on short definitions of a selection of terms and problems. This exercise is an opportunity to refresh your memory and will allow the class to proceed at an advanced level.

2. Exams (4 X 80 points = 320 points)

Exams will be a combination of fill-in-the-blank, short answer, essay and problem-solving. You will be expected to not only know definitions, but also to be able to apply your knowledge to answering questions using genetic approaches

3. Problem sets (7@ 10 pts each)

Problem sets will consist of 4-6 questions covering the essential concepts of the previous week. The idea is to get you thinking about how you could apply the material we cover in a new context. The problems will focus on: 1) molecular techniques – which one to use when? 2) genetics of the organism – what are the progeny and where did they come from? 3) genomics – what information is out there and how do you get it? Problems are due at the **beginning of class** on the due dates as listed on the schedule:

PLEASE NOTE: Once problem sets are turned in, we will go over the answers briefly in class. Therefore, late submissions will not be accepted (whether you attend class or not.)

4. In-class exercises (20 points)

Part of our time in class will be devoted to problem solving, thought questions, or other active learning exercises. Over the course, these are worth 20 points in total. You must be present in class – and participating – in order to earn the points. We are not offering make-up for these points.

5. Presentations (80 points):

Each of you will select a paper from a recent (2011-2012) Nature or Science or similar journal that needs to be approved by Dr. Garrity or Dr. Bedinger by October 24. The paper needs to be focused on a gene or set of genes. You will need to identify and READ at least three “support papers” including review articles, previous work etc. A one-page outline of your talk, including list of references, is due November 7. Each presentation should be 15 minutes in length. Practice, and time yourself (it may be helpful to get together with other class members for this). You should be using about 15 slides per presentation. Slides should be legible, interesting and tothe- point (don’t make them overly complex). Drs. Garrity and Bedinger will be happy to offer suggestions on drafts of talks, so long as you make appointments at least a week in advance of your talk.

6. EXTRA CREDIT OPPORTUNITY- Genetics in the News

A total of 10 extra credit points is possible for students presenting news articles about genetics (must include a genetic trait or gene or genome) to the class on Fridays (2 extra credit points for each presentation). Articles should have been published in the popular press (not technical journals) within the past 6 months, preferably even more recently. Presentations should not exceed 2 minutes each, and there will be a maximum of five presentations each Friday.

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• Published: 09 September 2024

Defining and pursuing diversity in human genetic studies

• Maili C. Raven-Adams 1 ,
• Tina Hernandez-Boussard   ORCID: orcid.org/0000-0001-6553-3455 2 ,
• Yann Joly   ORCID: orcid.org/0000-0002-8775-2322 3 ,
• Bartha Maria Knoppers   ORCID: orcid.org/0000-0001-7004-2722 3 ,
• Subhashini Chandrasekharan 4 ,
• Adrian Thorogood 5 ,
• Judit Kumuthini 6 ,
• Calvin Wai Loon Ho   ORCID: orcid.org/0000-0002-8328-1308 7 , 8 , 9 ,
• Ariana Gonzlez 10 , 11 ,
• Sarah C. Nelson   ORCID: orcid.org/0000-0002-2109-6465 12 ,
• Yvonne Bombard   ORCID: orcid.org/0000-0002-9516-4539 13 , 14 ,
• Donrich Thaldar 15 ,
• Hanshi Liu 3 ,
• Alessia Costa 16 ,
• Vijaytha Muralidharan   ORCID: orcid.org/0000-0003-0226-8468 2 ,
• Sasha Henriques 16 ,
• Jamal Nasir 17 ,
• Aimé Lumaka   ORCID: orcid.org/0000-0002-5468-8678 18 , 19 ,
• Beatrice Kaiser   ORCID: orcid.org/0000-0003-2227-9009 2 , 20 ,
• Saumya Shekhar Jamuar   ORCID: orcid.org/0000-0003-2341-8349 21 , 22 &
• Anna C. F. Lewis   ORCID: orcid.org/0000-0002-1274-386X 23 , 24  

Nature Genetics ( 2024 ) Cite this article

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Calls for more diverse data in genetics studies typically fall short of offering further guidance. Here we summarize a policy framework from the Global Alliance for Genomics and Health designed to fill this gap. The framework prompts researchers to consider both what types of diversity are needed and why, and how aims can be achieved through choices made throughout the data life cycle.

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Acknowledgements

The Diversity and Datasets taskforce acknowledges the contributions from other members of the Regulatory and Ethics Workstream, members of the public and other commenters who attended our many meetings. In particular, we acknowledge M. Afolabi, S. H. Chen, M. Doerr, J. S. Hsu, Z. Lombard, M. Mackintosh, A. Saadat and S. Singh. A.C.F.L. is supported by the NHGRI (1K99HG012809). S.S.J. is supported by National Medical Research Council, Singapore Clinician Scientist Award (NMRC/CSAINVJun21-0003)

Author information

Authors and affiliations.

Nuffield Council on Bioethics, London, UK

Maili C. Raven-Adams

Department of Medicine, Stanford University, Stanford, CA, USA

Tina Hernandez-Boussard, Vijaytha Muralidharan & Beatrice Kaiser

Centre of Genomics and Policy, Victor Phillip Dahdaleh Institute of Genomic Medicine, McGill University, Montreal, Quebec, Canada

Yann Joly, Bartha Maria Knoppers & Hanshi Liu

National Institutes of Health, Bethesda, MD, USA

Subhashini Chandrasekharan

The Terry Fox Research Institute, Vancouver, British Columbia, Canada

Adrian Thorogood

African Biobanks and Longitudinal Epidemiologic Ecosystem, Ibadan, Nigeria

Judit Kumuthini

Faculty of Law, Monash University, Melbourne, Victoria, Australia

Calvin Wai Loon Ho

Centre for Medical Ethics and Law, University of Hong Kong, Hong Kong, China

PHG Foundation, University of Cambridge, Cambridge, UK

Genoox, Tel Aviv, Israel

Ariana Gonzlez

Bioethics Institute, Medical Science Department, Pontifical Catholic University (UCA), Buenos Aires, Argentina

Department of Biostatistics, University of Washington, Seattle, WA, USA

Sarah C. Nelson

Institute of Health Policy, Management and Evaluation, University of Toronto, Ontario, Canada

Yvonne Bombard

Genomics Health Services Research Program, St Michael’s Hospital, Unity Health Toronto, Ontario, Canada

School of Law, University of KwaZulu-Natal, Durban, South Africa

Donrich Thaldar

Connecting Science, Wellcome Genome Campus, Hinxton, UK

Alessia Costa & Sasha Henriques

Life Sciences, University of Northampton, Northampton, UK

Jamal Nasir

Centre for Human Genetics, University of Kinshasa, Kinshasa, Democratic Republic of the Congo

Aimé Lumaka

African Rare Disease Initiative https://www.ardi.africa/

Global Alliance for Genomics and Health https://www.ga4gh.org/

Beatrice Kaiser

SingHealth Duke–NUS Institute of Precision Medicine, Singapore, Singapore

Saumya Shekhar Jamuar

Department of Paediatrics, KK Women’s and Children’s Hospital, Singapore, Singapore

Division of Genetics, Brigham and Women’s Hospital, Boston, MA, USA

Anna C. F. Lewis

Harvard Medical School, Boston, MA, USA

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Corresponding author

Correspondence to Anna C. F. Lewis .

Ethics declarations

Competing interests.

A.C.F.L. owns stock in Fabric Genomics. T.H.-B. reports consulting fees from Grai-Matter and Paul Hartmann AG outside the submitted work. Y.B. owns stock in Genetics Adviser. S.S.J. is a co-founder of Global Gene Corporation. The other authors declare no competing interests.

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Raven-Adams, M.C., Hernandez-Boussard, T., Joly, Y. et al. Defining and pursuing diversity in human genetic studies. Nat Genet (2024). https://doi.org/10.1038/s41588-024-01903-7

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Select committee report on contracts of insurance bill.

• The latest version of the Bill includes power to make regulations regarding the use of genetic testing by insurers
• The Bill clarifies that premiums payable are excluded from unfair contract terms in respect of life and health insurance policies
• Reinsurance contracts are also clearly carved out from the scope of the regime 
• The threshold for misrepresentation has been reframed as ‘dishonest’ rather than ‘fraudulent’ with dishonest misrepresentation being taken as showing lack of reasonable care
• Timing for the implementation of the Bill is still to be confirmed.

Introduction

The Finance and Expenditure Committee has reported back on submissions received on the Contracts of Insurance Bill. In this Financial Law Insight we break down some of the key issues identified by submitters, how the Committee responded, and its recommendations for the Bill. 

The story so far

The Contracts of Insurance Bill (Bill), introduced to Parliament on 29 April 2024 by Hon Andrew Bayly (after a rebrand of the previous Insurance Contracts Bill), signifies a long awaited reform to New Zealand’s insurance contracts law.

To recap, the proposed changes set out in the Bill include:

• A new duty of disclosure: for consumer insurance contracts – those wholly or predominantly for personal, domestic, or household purposes – policyholders will have a duty to take reasonable care not to make a misrepresentation to the insurer. For non-consumer insurance contracts, policyholders will have a duty to make a fair presentation of the risk.
• Proportionate remedies: rather than wholly avoid a contract for the policyholder’s failure to disclose, insurers will instead need to respond proportionately, based on the how they would have acted had the information been known at the time of entry into the contract.
• Codified and modified duty of good faith: the Bill modifies the duty of utmost good faith so that a consumer insurance policyholder is only under a duty to take reasonable care not to make a misrepresentation (or a duty to make a fair presentation of risk in respect of non-consumer insurance contracts). Insurers will no longer be able to avoid a contract on the basis utmost good faith has not been observed.
• Clear, concise, and effective: insurers will be required to ensure insurance contracts are worded and presented in a clear, concise, and effective manner.
• Claims paid within a reasonable time: a new implied term included in insurance contracts that insurers must pay claims ‘within a reasonable time’.
• Unfair contract terms: a narrowing of existing exemptions from the Fair Trading Act unfair contract terms for insurance contracts.  

Key issues identified by Select Committee

The Finance and Expenditure Committee (Committee) has now released its report on the Bill . Initially, the Committee expressed particular interest in receiving written submissions on:

• what is a ‘reasonable’ timeframe for resolving claims
• whether the policyholder disclosure duty is sufficiently clear and plain language
• provisions around surrender values for life insurance policies.

Submitters also called for greater consideration of several other matters in the Bill. These issues, which the Committee responded to, were in relation to:

• genetic discrimination in life and health insurance
• the definition of ‘specified intermediary’
• disclosure duties for consumer and non-consumer insurance contracts
• duties of brokers in relation to premiums and payments due to the policyholder
• the need to exclude premiums payable from ‘unfair contract terms’.

Genetic discrimination in life and health insurance

Several submitters brought to the Committee’s attention the issue of ‘genetic discrimination’ in the context of life and health insurance – being instances where insurers treat consumers differently based on genetic testing results. The Bill (as introduced) was silent on this issue, and it is not addressed by either existing law or government policy. 

The Committee agreed on the importance of the issue, noting that a cautionary approach to genetic testing is needed to avoid undue genetic discrimination. 

The Committee recommended inserting new regulation-making powers that could prohibit or regulate the conduct of insurers in connection with genetic testing. The Bill provides a non-exhaustive list of conduct that could be regulated, including:

• whether an insurer can require a person to undergo or consent to, or disclose the results of, a genetic test or answer a question about whether they have undergone any genetic test
• whether an insurer can refuse to engage with a person due to the above factors
• what may be taken into account by an insurer. 

Specified intermediaries

The Bill subjects ‘specified intermediaries’ to certain duties – for example, in relation to consumer insurance contracts, specified intermediaries must take reasonable steps to pass on a policyholder’s representation to the insurer before the insurer enters into or agrees to vary the contract.

Submitters argued, and the Committee agreed, that the narrow definition of ‘specified intermediary’ would only capture those who receive a commission or other incentive directly from an insurer. It would not capture financial advisers engaged by financial advice providers (FAP) (in cases where FAPs receive commissions from insurers, and then pay their financial advisers). 

The Committee recommended broadening this definition to include intermediaries who receive a commission or consideration directly or indirectly from an insurer. This ensures financial advisers are also covered by the duties imposed on specified intermediaries.

Are the disclosure duties clear enough?

‘reasonable care’ duty for consumer insurance contracts.

The Bill proposes a new disclosure duty on policyholders of consumer insurance contracts to take ‘reasonable care’ not to make a misrepresentation to the insurer before the consumer insurance contract is entered into or varied. 

Submitters were generally supportive of the amended duty that requires policyholders to take reasonable care not to make a misrepresentation. 

A common sentiment among industry submitters was that the Bill’s ‘weighing up exercise’ to determine reasonable care creates uncertainty. Greater clarity is required for insurers to ascertain the appropriate questions to ask before entering into a contract. The Committee disagreed with this and considered that the Bill uses appropriate language for a statutory duty, and that the duty on insurers to inform a policyholder of the general nature and effect of the policyholder’s disclosure duty could include ‘explaining what this means in practical terms’. 

More significantly, the Committee recommended replacing ‘fraudulent’ misrepresentation (which is always taken to mean lack of reasonable care) with ‘dishonest’ misrepresentation. 

Submitters argued that a broadening of the threshold is necessary to refer to actions that are not honest or lack integrity, without always involving deliberate deception with the intent to secure an unfair or unlawful gain. The Committee agreed on the basis that the term ‘dishonest’ is appropriate, consistent with the approach in the United Kingdom, and avoids associations with criminal standards. 

The Bill also tidies up what matters may be taken into account by an insurer when determining whether a policyholder has taken reasonable care not to make a misrepresentation. 

The Bill includes a clause that provides where a policyholder fails to answer a question or gives an obviously incomplete or irrelevant answer, then any steps the insurer took in response to that failure or inadequate answer will be taken into account. This clearly places the onus on the insurer to take additional steps if a non-answer is given or an answer is obviously incomplete or irrelevant.

‘Fair presentation of the risk’ duty for non-consumer insurance contracts

The Bill sets out a different disclosure duty for policyholders of non-consumer insurance contracts. In this case, policyholders must make a ‘fair presentation of the risk’ before entering into the non-consumer insurance contract. However, a policyholder is not required to disclose a circumstance if the insurer knows, ought to know, or is presumed to know the circumstance.

Submitters argued for the removal (or, at least, the narrowing) of the presumption that an insurer is taken to ‘know’ something if it is known to any individual who participates in the decision whether to take the risk on behalf of the insurer, or any individual who is, or works for, a specified intermediary ‘in relation to the contract of insurance’. 

Some submitters argued that the insurer should only be deemed to know what has been disclosed to them (or the specified intermediary) by the policyholder. The Committee disagreed on this specific point, but proposed to amend the clause to make clear it is intended to apply to individuals who are or who work for a specified intermediary in relation to that insurance contract (and not to other employees whose work is unrelated to that specific contract). 

‘Reasonable’ timeframe to resolve claims

The Bill proposes to introduce an implied term into every insurance contract that an insurer must pay out a claim within a ‘reasonable time’. The previous Insurance Contracts Bill provided a specified 12-month reasonableness period which, if not met, would have resulted in interest payable on any outstanding claims from that date.

Submitters supported removal of a specified time period, and were of the view that an open-ended reasonableness standard would allow insurers to take into account a range of factors specific to their context. The Committee recommended expanding the ambit of ‘reasonable time’ to include reasonable time to gather information needed to investigate and assess the claim.

Duties of brokers in relation to premiums and payments due to the policyholder

The Bill imposes a duty on brokers to pass on to the insurer any premiums that they receive from a policyholder within a ‘relevant period’. The Bill clarifies that this does not prevent insurers from making a contract or an arrangement with a broker to vary this period.

Submitters queried whether this would retrospectively allow for variations to be agreed to existing arrangements, to save existing arrangements from being renegotiated. The Committee agreed that any existing agreements that vary the timeframe for payment should continue to apply. A ‘grandfathering provision’ is now set out in the Bill to make clear that existing contracts or arrangements of this kind will continue in effect after commencement of the Bill.

Separately, the Committee also recommended removing the criminal offence for failure to pass on premiums as outlined above, and instead providing that the relevant insurer may recover in Court as a debt due any amounts not passed on by a broker under the duty.

Payments due to the policyholder

The Bill imposes a further duty on brokers to pass on to the policyholder any payments made by the insurer within seven days of the broker receiving the money. The Committee recommended a limited amendment to now require brokers to pay policyholders of non consumer insurance contracts ‘as soon as reasonably practicable’ rather than within seven days. This permits a degree of flexibility for commercial insurance arrangements that can be more complex than consumer ones.

Excluding premiums from unfair contract terms

The Bill will amend the Fair Trading Act to remove some exemptions from the unfair contract terms provisions of that Act that currently apply to insurance contracts. 

Submitters argued, and the Committee agreed, that the list of terms to be excluded from being unfair contract terms should also include a term relating to the amount of a premium payable in the context of life and health insurance contracts. This aligns insurers of life and health policies, which adjust premiums on annual policy anniversaries, with general insurers whose contracts renew (and are repriced) on an annual basis.

Surrender values for life insurance policies

The Bill carries over existing provisions in relation to surrender values, allowing a life insurer to apply the surrender value of a life policy in payment of overdue premiums and interest. As long as overdue amounts do not exceed that value, the policy is not void because of the non-payment. 

The Committee expressly requested feedback for this area, however the submitters that provided feedback were supportive of these provisions and did not suggest any changes be made. The Committee considered it appropriate to retain these provisions unchanged. 

Other amendments recommended

In addition to technical changes, the Committee recommended several other useful amendments to the Bill. These include:

• excluding contracts of reinsurance from the Bill (by expressly excluding such contracts from the definition of contract of insurance)
• removing the presumption that an insurance contract is a consumer insurance contract
• amending the ‘conflict of laws’ provision to allow for parties to a non-consumer insurance contract to have the autonomy to choose which law governs their contracts (not limited to New Zealand law)
• changing ‘all reasonable steps’ to ‘reasonable steps’ regarding an insurer’s need to ensure that policyholders are informed of certain matters such as the duty of disclosure and accessing third party information
• clarifying that compliance with the duties in the Bill does not place specified intermediaries in breach of any contract 
• clarifying that life insurers may charge a higher premium for the remainder of the contract if the insurer would have entered into a contract on different terms but for a qualifying misrepresentation or breach by the policyholder.

The Bill is currently at the second reading stage. The House will now debate and vote on any changes suggested by the Committee. This will determine its fate, as the House will be asked to adopt the Bill before it ‘in principle’. 

With the Bill being close to final form, a key consideration now will be planning for its implementation. This includes timing of key obligations. 

We had suggested a two year transition period at a minimum. Officials have noted that more than 12 months’ lead time will be needed for the significant set up work required for many of the substantive changes in the Bill, including the new disclosure duties. However, the determination of the commencement dates has been left to a later phase after the Bill is in the final legislative stages. Helpfully, further engagement with ‘stakeholders’ will be undertaken on timing.

Start a conversation 

If you would like to discuss any aspect of the insurance law reforms or any other financial services matter, please contact David Ireland on +64 4 498 0840, Catriona Grover on +64 4 498 0816, Tom McLaughlin on +64 9 892 5215, or Mark Schroder on +64 9 375 1120 or email the team at [email protected] .

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