eyes open – 第 2 页

Mendel’s Genetics [7]: handling problems

In college, while learning genetics, you may be faced with data obtained from F1 and F2 generations of the crosses. And you are required to be able to recognize ratios in order to decide how many genes are involved, and whether or not epistasis (which we talked about last section) is taking place.

Example(1)

A cross between two pure-breeding white-fruited tomato plants produced and F1 generation which all plants had purple fruit. In the subsequent F2 generation 160 plants were obtained; of these 94 had purple fuit, and the rest had white fruit.

As we know nothing about the genes controlling fruit color in tomato, we must first ask ourselves a question: “DOES THE DATA FIT ANY OF THE KNOWN MENDELIAN RATIOS?”

Since only two phenotypes are involved, it can’t be 9:3:3:1, or 9:3:4 or any mendelian ratios with more than 2 numbers included.

On examination of ratios with 2 phenotypes, 9:7 looks like a possible candidate, but 3:1 may also fit.

In this case, to decide which is the best to fit the data, we introduce a new approach to this problem: the Chi-square test.

Chi-square( test)=
sum[(obseved expected)ˆ2/expected]

(Xˆ2 is always calculated from original data, never from percentages, frequencies or proportions.)

If Xˆ2 is large, the data doesn’t fit. A perfect fit gives Xˆ2 a zero. BUT HOW LARGE IS LARGE?

In addition to the result of Xˆ2, we need another piece of info to determine “how large is large”. We need to know the degrees of freedom.

Degrees of freedom are one less than the number of classes. They tell us something about the number of independent numbers we have, which relates to the usefulness of our data.

In this example, we have two phenotypic classes, purple, and white. It means when we have counted the purple ones, the number of the white ones is fixed so we have only one degree of freedom.

If we had three classes, we would have two degrees of freedom: when the two classes have been counted, the number of the third is fixed.

As the degrees of freedom gets bigger, Xˆ2 gets bigger. So the answer of HOW LARGE IS LARGE depends on different degrees of freedom.

In this example, we determine which ratio is the best fit by comparing the value of Xˆ2

Observed result: 94 purple 66 white

Result predicted by 9:7 ratio 160×9/16 =90 160×7/16 =70

Xˆ2=[(94-90)ˆ2/90]+[(66-70)ˆ2/70]=0.41,with one degree of freedom

Result predicted by 3:1 ratio 160×3/4=120 160×1/4=40

Xˆ2=[(94-120)ˆ2/120]+[(66-40)ˆ2/40]=22.5,with one degree of freedom

Using Xˆ2 probability tables can help quickly get to the value of Xˆ2.

the x2 ditribution table — X2 PROBABILITY TABLE, from “Instant Notes in Genetics”

How to use it?

Follow the line for the one degree of freedom(top line) to find the nearest values of xˆ2 above and below our value.

We can see that the value of 0.41 is between the probability of 0.975 and 0.050 with an affinity to 0.975, which means that if we repeated the experiment 1000 times, we have a probability close to 97.5% that the observed ratio would fit 9:7. The value of 22.5 is way beyond way exceeded with the probability of 0.001, which suggests that 3:1 ratio doesn’t fit the data.

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Data analysis after class:

A cross between pure-breeding white-fruited and purple-fruited tomato plants produced and F1 generation which all plants had purple fruit. In the subsequent F2 generation 160 plants were obtained; of these 99 had purple fuit, 25 had red fruit, and 36 had white fruit.

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卡方检验是以χ2分布为基础的一种常用假设检验方法，它的无效假设H0是：观察频数与期望频数没有差别。

该检验的基本思想是：首先假设H0成立，基于此前提计算出χ2值，它表示观察值与理论值之间的偏离程度。根据χ2分布及自由度可以确定在H0假设成立的情况下获得当前统计量及更极端情况的概率P。如果P值很小，说明观察值与理论值偏离程度太大，应当拒绝无效假设，表示比较资料之间有显著差异；否则就不能拒绝无效假设，尚不能认为样本所代表的实际情况和理论假设有差别。

the blueprint of life [7]: prokaryotic chromosome structure of DNA

First, let’s make sure the anatomy of prokaryotes are familiar to us:

Prokaryotes are the simplest living cells, typically 1~10μm in diameter, and are found in all environmental niches from the guts of the animals to acidic hot springs.

They are bounded by a cell (plasma)membrane comprising a lipid bilayer, in which are embeded proteins that allow the exit and entry of small molecules.
Most prokaryotes also have a rigid cell wall outside the plasma membrane, which prevents the cell from swelling or shrinking in environments where osmolarity differs significantly from that inside the cell.
Sometimes the cell wall is surrounded by an (often) polysaccharide envelope called capsule.
The cell interior (cytoplasm or cytosol) usually contains a single, circular chromosome compacted into a nucleoid and attached to the membrane.
There are no distinct subcelluar organelles in prokaryotes as in eukaryotes(except for the ribosomes核糖体).
The surface of a prokaryote may carry pili, which allow the prokaryote to attach to other cells and surfaces. Some prokaryotes also carry flagella, whose rotating motion allows the cell to swim.

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To talk about prokaryotic chromosome structure, we use E. coli (大肠杆菌)as the example.

E. coli chromosome contains a single supercoiled circular DNA molecule of length 4.6 million bp.
E. coli chromosome is highly folded: 1500 µm of DNA length versus ~1 µm of cell size, forming a structure called the nucleoid.
The nucleoid has a very high DNA concentration, perhaps 30~50 mg/ml, as well as containing all the proteins associated with DNA, such as polyerases, repressors(a protein that is determined by a regulatory gene, binds to a genetic operator, and inhibits the initiation of transcription of messenger RNA), etc.

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DNA domains (loops)

Remember this famous electron micrograph of an E. coli cell we showed before? The cell was carefully lysed, all the proteins removed and then, it was spread on an EM grid to reveal all of its DNA.

Several of such experiments revealed one level of organization of the nucleoid.

The DNA consists of 50~100 domains or loops, about 50~100 kb in size (kb: kilobase, a unit of measure of the length of a nucleic-acid chain that equals one thousand base pairs).
The ends of the loops are constrained by binding to a structure which probably consists of proteins attached to part of the cell membrane.
Not known whether the loops are static or dynamic, but one model suggests that the DNA may spool(wind) through sites of polyerase or other enzymic action at the base of the loops.

E coli DNA instant notes

image above is from”Instant Notes in Molecular Biology”

Supercoiling of the genome

The E. coli chromosome as a whole is negatively supercoiled, although there is some evidence that indicates individual domains may be supercoiled independently. Electron micrographs indicate that some domains may not be supercoiled, perhaps because the DNA has become broken in one strand, where other domains clearly do contain supercoils.

The domains may be topologically independent. There is, however, no real biochemical evidence for major differences in the level of supercoiling in different regions of the chromosome in vivo

DNA-binding proteins

The looped DNA domains of the chromosome are constrained further by inter-action with a number of DNA-binding proteins.

The most abundant of these are protein HU, a small basic (+charged) dimeric protein, which binds DNA non-specifically by the wrapping of the DNA aorund the protein.

And H-NS (formerly known as the protein H1), a monomeric neutral protein, which also binds DNA non-specifically in terms of sequence, but seems to have a preference for regions of DNA which are intrinsically bent.

These proteins are sometimes known as histone-like proteins, and have the effect of compacting the DNA, which is essential for the packaging of the DNA into the nucleoid, and of stabilizing and constraining the supercoiling of the chromosome.

the blueprint of life [6]: Chromosomal Structure of DNA 1

vocabulary

•Nucleus: 细胞核; Nucleolus: 核仁; Nucleoid: 类核

• Mitosis: 有丝分裂; Meiosis: 减数分裂

Interphase: 分裂间期; Prophase: 分裂前期; Metaphase: 分裂中期; Anaphase: 分裂后期; Telophase: 分裂末期

• Histone: 组蛋白

• Nucleosome: 核小体

•Chromosome: 染色体; Chromatin: 染色质; eu- 真染色质; hetero- 异染色质

• Centromere: 中心粒; Telomere: 端粒

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WHAT is chromosome:

Structure containing the genes of a cell and made of a single DNA molecule and its associated proteins.

CHROMOSOMES OF EUKARYOTES, shown by prof. Dong

HOW long is DNA in an chromosome
HOW LONG IS DNA, shown by prof. Dong.

→A chromosome is too long to fit into a cell without compaction.

WHY is DNA packed into chromosomes

Chromosome is a compact form of the DNA that readily fits inside the cell
To protect DNA from damage
DNA in a chromosome can be transmitted efficiently to both daughter cells during cell division
Chromosome confers an overall organization to each molecule of DNA, which regulates gene expression as well as recombination

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Diversity of chromosomes

in terms of:

Shape: circular or linear
Number: species-specific

eg. -fruitfly 8; -human 46; -horse 64; -dog 78; -chicken 78

-maize 20; -rice 24; -wheat 42

Copy number: haploid单倍体, diploid双倍体, polyploid 多倍体

Overall structure: highly different between prokaryotes 原核生物and eukaryotes真核生物

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Next section we will first talk about prokaryotic chromosome structure of DNA.

Flight Behavior: What Is The Use of Saving A Planet That Has No Soul Left In It?

World consumption of paper has grown 400 percent in the last 40 years. Now nearly 4 billion trees or 35 percent of the total trees cut around the world are used in paper industries on every continent.(source)

For the trees’ sake, please please please please use e-books!

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Flight Behavior by Barbara Kingsolver
Pages: 448
Release Date: November 6, 2012
Publisher: Harper
Genre: Literary Fiction

A novel you wouldn’t put down once opening the first page.

Barbara wrote with close attention to language and intelligent arrangement of plot. Only having read the first chapter, you would never get right what the novel is really about.

Generally, the 2012 novel focuses on the interactions between humans and the natural environmental they are living in, which leads to a core topic of today’s environmental situation:climate change. But not like what we read in Science, where climate change is drawn in a scientific way. No logical reasoning, non data analysis, climate change in Flight Behavior is lyrically written, tragic, sad, forcing innocent monarch butterflies abandon their hometown (also original wintering habitat) and flew all the way to a small town in southern U.S for survival.

Family matters, communities, scientists, butterflies, climate change, meanings of life, faith…

No more spoilers, hope you enjoy this book and after reading it, would see more respects in environmental conservation.

Mendel’s Genetics [6]: Examples of epistasis

In Mendel’s dihybrid cross, each gene locus(the position of a gene along a chromosome, often used to refer to the gene itself.) had an independent effect on a single phenotype. Thus, the R and r alleles affected only the shape of the seed and had no influence on seed color, while the Y and y alleles affected only seed color and had no influence on seed shape. In this case, there were two separate genes that coded for two separate characteristics.

But what happens when two different loci affect the same characteristic? For instance, what if both of the loci in Mendel’s experiment affected seed color?

Let’s begin with a relatively simple example.

example (1) 9:3:3:1→9:7

enzyme A serves to convert white substrate in an unnamed plant to white product; enzyme B synthesizes purple pigment and converts the white product to purple product.

In this case, If BOTH A & B exist, purple product is yielded;

If ONLY A OR B exists, synthesis of purple pigment cannot be completed, and purple product won’t be produced;

If NEITHER ENZYME exist, purple pigment, surely, cannot be synthesized, and purple product won’t be produced.

Based on the info above, the dihybrid F2 generation looks like this:

When the situation gets a little bit more complicated:

example (2) 9:3:3:1→9:3:4

enzyme A serves in the synthesis of red pigment and converts white substrate in an unnamed plant to red product; enzyme B synthesizes purple pigment and converts the red product to purple product.

In this case, If BOTH A & B exist, purple product is yielded;

If ONLY A exists, synthesis of red pigment can be completed but synthesis of purple pigment cannot, and red product will be produced;

If NEITHER ENZYME exist or ONLY B exists, surely, neither red or purple pigment, can be synthesized, and the the yield will be white.

Based on the info above, the dihybrid F2 generation looks like this:

A more complex situation:

example (3): 9:3:3:1→12:3:1

Here two enzymes compete for the same substrate. Enzyme A converts the substrate to a purple product, and enzyme B to a red product. BUT enzyme A has much higher affinity for the substrate than enzyme B. The difference in affinity is so marked that enzyme B can only work effectively without the presence of enzyme A

SO as long as enzyme A is present, the yield is be purple; only when enzyme B exists without enzyme A would the yield be red; and only when neither B or A exists would the yield be white.

Based on the info above, the dihybrid F2 generation looks like this:

[F2] purple: red: white=12: 3: 1

The three examples above lead us to a new concept: Epistasis.

Sometimes genes can mask each other’s presence or combine to produce an entirely new trait. Epistasis describes how gene interactions can affect phenotypes.

In a strict sense, 12: 3: 1 is the only ratio which was originally referred to as epistasis, because the presence of enzyme A can completely make the genotype of the B gene. But the term is now used wherever genes interact to alter the expected ratios.

There are several other variations of the 9:3:3:1 ratio caused by interaction between the gene products, including 9:6:1, 15:1, and 13:3.

In every case the ratios are derived by summing together the four phenotype classes 9, 3, 3, or 1 of the basic ratio.

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For more examples and explanations of the Epistasis, see Epistasis and Its Effects on Phenotype | Learn Science at Scitable

The blueprint of life [5]: spectroscopic and thermal properties of DNA

UV absorption

DNA absorbs UV light due to the conjugated aromatic nature of the bases; the sugar-phosphate backbone does not contribute appreciably(perceptibly/measurably) to absorption.

The wavelength of maximum absorption of light by both DNA and RNA is 260 nm, which is conveniently distinct from the λmax of protein(280 nm).

The absorption properties of DNA can be used for detection, quantitation and assessment of property.

Hypochromicity

UV absorption at 260nm is greatest for isolated nucleotides, intermediate for single-stranded DNA(ssDNA) or RNA, and least for double-stranded DNA(dsDNA)

The classical term for the change in absorbance is hypochromicity. For example, dsDNA is hypochromic (from the Greek for ‘less colored‘) relative to ss DNA, which is hypochromic relative to isolated nucleotides.

Thermodynamics of DNA

Denaturation: the transition of macromolecule from the native state to the denatured state. For DNA, under denaturing conditions (heating or high pH), double helix is separated to generate single-stranded form.

Melting Temperature(Tm): the temperature at which the rise in A260(absorbance at 260nm) is half complete during denaturation.

Factors that affect the Tm

1. G+C content: the higher G+C content, the higher Tm.

2. Ionic strength: The Tm increases as the cation (+) concentration increases. like Na+, K+ or Mg2+.

3. High pH or Agents that disrupt H-bonds or interfere with base stacking: formamide (甲酰胺)or urea (尿素)will decrease the Tm.

4. The imperfect hybridization between related but not completely complementary strands will reduce the Tm, about 1 °C for each percent mismatch.

The process of denaturation can be observed conveniently by the increase in absorbance as double-stranded nucleic acids are converted to single strands

Renaturation: Process of a macromolecule returning to its native 3-D structure. For DNA this involves the two strands of denatured DNA basepairing to restore the nature form of dsDNA. Also known as reannealing (重退火).

Requirements for renaturation:

1. Proper salt concentration: neutralize electrostatic repulsion

2. Proper reannealing temperature: 20-25℃ below Tm

Determinants for renaturation efficiency

(DNA renatures on cooling, but will form fully double-stranded native DNA only if the cooling is sufficiently slow to allow the complementary strands to anneal.)

1. Extent of base matching and

2. copy of matching regions

Thus, repetitive DNA renatures faster than single copy DNA

RENATURATION CURVES FOR E.COLI &MOUSE DNA, shown by prof. Dong

Mendel’s Genetics [5]: The dihybrid cross

Last sections we discussed inheritance where only a single gene was involved. The 3:1 ratio is the basic Mendelian ratio and everything that follows depends upon it.

The obvious next step is to look at a situation where the inheritance of two different inherited characters are studied at the same time, a dihybrid cross.

Again, we learn dihybrid cross by experiments. Let’s see what Mendel did:

He crossed two pure-bred starins of pea plants, one producing only round yellow seeds and the other only wrinkled green seeds.Round seeds are dominant over wrinkled ones; yellow seeds are dominant over green ones. Both phenotypes are determined by one single gene.

(Why did Mendel use the seed characteristics as his focus of study instead of other traits of the pea plants? )

A cross between the two parents produced a F1 generation that consisted only of round yellow seeds. Self-fertilization of F1 yielded F2 generation, the seeds of which showing considerable diversity.

Four different phenotypes could be identified. Of 556 seeds analyzed, Mendel found 315 round yellow seeds, 108 round green seeds, 101 wrinkled yellow seeds and 32 round green seeds. Close to a ratio of 9: 3: 3: 1, which is referred to as the dihybrid ratio.

dihybrid cross — THE 9:3:3:1 IN MENDEL’S EXPERIMENTS, image from Instant Notes in Genetics

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Interestingly, if we only focus on the round/wrinkled phenotype, the ratio of round seeds and wrinkled seeds is 3:1. the monohybrid ratio. Similarly, if we only focus on the yellow/green phenotype, the ratio of yellow seeds and green seeds is the monohybrid ratio as well. Just as we said “The 3:1 ratio is the basic Mendelian ratio and everything that follows depends upon it”

Now I want to introduce a little bit mathematics into this section. Let’s see what happens when we use polynomial multiplication to explain the relationship between 9: 3: 3: 1 and 3:1:

(yellow: green)× (round: wrinkled)

= (yellow·round): (yellow·wrinkled): (green·round): (green·wrinkled)

known: yellow: green=3:1; round: wrinkled=3:1

SO: (yellow: green)×(round: wrinkled)=(3:1)×(3:1)

=(3×3):(3×1):(1×3):(1×1)=9:3:3:1

Therefore, (yellow·round): (yellow·wrinkled): (green·round): (green·wrinkled)=9:3:3:1
Does this reasoning inspire you? What happens when it comes to a tri-hybrid ratio?

(3:1)×(3:1)×(3:1)=

(3×3×3):(3×3×1):(3×1×3):(3×1×1):(1×3×3):(1×3×1):(1×1×3):(1×1×1)

=27 : 9 : 9 : 9 : 3 : 3 : 3 : 1

See? Quite easy. The ratios for the three groups of phenotypes are simply multiplied across, and the 27 : 9 : 9 : 9 : 3 : 3 : 3 : 1 ratio is obtained.

SO what happens when it comes to tetra-hybrid, penta-, hex-? What happens when it comes to n-hybrid?

I’m sure the answer is easy for you now, make the n phenotypes multiplied across, and the expected ratio is obtained. In plain mathematics, (3:1)^n

——————————————————————————-As noted before the 3:1 ratio can be distorted by factors such as incomplete dominance or lethal alleles. These also affect the 9:3:3:1 ratio, but other factors can also modify this ratio.

The two different genes must not act on the same character. For instance, if the proteins encoded by the two genes are involved in the same biochemical pathway then the ratios of phenotypes resulting from the genotypes will be altered.
If the two genes lie close together on the same chromosome, linkage happens and the ratio won’t be 9:3:3:1 either, as we mentioned in Review of Mendel’s Genetics, the very beginning of our Genetics study.

Testcross

As with the monohybrid cross, it is also possible to conduct a testcross with F1 generation of the dihybrid cross.

The blueprint of life [4]: Tertiary Structure of DNA

Finally, we come to the last part of the molecular structure of DNA.

4. Tertiary Structure of DNA – superhelix structure

Advanced folding and intertwining of DNA molecules over the secondary structure .

DNA topology

1. Linear DNA:

Commonly seen in eukaryotes,
with extreme length,
complementary sequence
included in the chromatin (the combination or complex of DNA and proteins that make up the contents of the nucleus of a cell)
interacting with other cellular components.

2. Circular DNA:

(DNA frequently occurs in nature as closed-circular molecules, where the two single strands are each circular and linked together. The number of links is known as the linking number(Lk).)

Usually seen in prokaryotes, e.g. plasmid (质粒), circular bacterial chromosomes and many viral DNA molecules
cccDNA (covalently closed circular DNA) → supercoiled or Relaxed; ncDNA (nicked circular DNA): a nick (缺刻)formed by breaking one phosphodiester bond
two complementary single strands are each joined into circles, 5′ to 3′, and are twisted around one another by the helical path of DNA.
The molecule has no free ends and the two single strands are linked together a number of times corresponding to the number of double-helical turns in the molecule.

cccDNA Topology

Supercoiled DNA

Negative superhelix: natural status of cccDNA with less intra- molecular tension (underwound effect)

Positive superhelix: unnatural status with higher tension (overwound effect)

Relaxed circular DNA: intermediate between negative superhelix and positive superhelix

Topological Equation of cccDNA

L = T + W

L=Linking number=total number of times one strand of the double helix links the other

T=Twisting number= the number of times one strand completely wraps around the other strand

W=Writhing number= the number of times that the long axis of the double helical DNA crosses over itself in 3-D space

Features

1. The linking number of a closed-circular DNA is a topological property, that is one which cannot be changed without breaking one or both of the DNA backbones. (A molecule of a given linking number is known as a topoisomer. Topoisomers differ only in their linking number)

2. Twisting number

For B DNA, T>0(10 bp per turn)

For A DNA, T>0(10.5 bp per turn)

For Z DNA, T<0 (12 bp per turn)

3. Writhing number

Relaxed: W=0

Negative supercoils: W<0

Positive supercoils: W >0

TWIST &WRITHE, from Instant Notes in Molecular Biology(3rd edition)

Topoisomerases (enzymes used to regulate the level of supercoiling of DNA molecules)

To alter the linking number of DNA, the enzymes must transiently break one or both stands. There are two classes of topoisomerases:

Type I Topoisomerase nick one strand of the DNA, changing 1 Linking-number at a time(+/-1 Lk)

Type II Topoisomerase, which requires the hydroloysis of ATP, break two strands of DNA, changing 2 Linking-number at a time(+/-2Lk); also able to unlink DNA molecules.

Most topoisomerases reduce the level of positive or negative supercoiling, that is, they operate in the energetically favorable direction. (However, DNA gyrase, a bacterial type II enzyme, uses the energy of ATP hydrolysis to introduce negative supercoiling into hence removing positive supercoiling generated during replication.)

Topoisomerases are essential enzymes in all organisms; they are involved in replication, recombination and transcription.

Both type I and II enzymes are the target of anti-tumor agents in humans.

DNA superhelix

Biological significance of Superhelix:

DNA packing:

Eg.

This is a famous electron micrograph of an E. coli cell that has been carefully lysed, then all the proteins were removed, and it was spread on an EM grid to reveal all of its DNA.

DNA functioning:

Negative supercoils serve as a store of free energy that aids in processes requiring strand separation, such as DNA replication and transcription; Strand separation can be accomplished more easily in negatively supercoiled DNA than in relaxed DNA.

1. DNA in cells is negatively supercoiled;

2.(-)supercoiling introduced by a topoisomerase II (gyrase 促旋酶) in prokaryotes and by nucleosome (核小体)in eukaryotes

3.Cruciform or bubble structures introduced by (-) supercoiling are potential protein-binding sites

Mendel’s Genetics [4]: examples of mutiple alleles

All the examples used in last classes have employed genes with only two alternative alleles. But the majority of genes exist in several different forms, multiple alleles. This is caused by the mutations of bases at different sites within the same gene, thus affecting different amino acids in the encoded protein.

examples of multiple-allele traits/diseases:

the human β-globin gene where a specific mutation at one site of the gene results in an allele responsible for the hereditary syndrome sickle cell (picture)anaemia, while mutations at several other sited sites in the gene cause a different syndrome, β-thalassemia(beta地中海贫血),
A SICKLE CELL,image from the Internet

Beta-thalassemia, inherited blood disorder caused by reduced or absent synthesis of the beta chains of hemoglobin, resulting in variable phenotypes ranging from severe anemia to clinically asymptomatic individuals.

Although they are alterations of the same gene, the changes are to different codons(a specific sequence of three consecutive nucleotides that is part of the genetic code and that specifies a particular amino acid in a protein or starts or stops protein synthesis). The resulting proteins have variant beta-globins with discrete differences in amino acid sequence and so behave differently.

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In rabbits, multiple alleles of one gene are responsible for a number of different coat color phenotypes.

Here we go, a little confusing but, interesting:

There are four members of the allelic series: agouti, chinchilla, Himalayan and albino. When homozygous, each series produces a distinct coat pattern. When heterozygous, there is a clear pattern of dominance. Agouti is dominant over all the alleles, chinchilla is dominant over Himalayan and albino, while Himalayan is dominant over albino, which fails to produce any pigment and hence is recessive to the others…Hope your mind is still clear!

1, Agouti rabbit: the wild rabbit.

genetics 4 an agouti rabbit — AN AGOUTI RABBIT, image form the Internet

If you blow into the fur of an Agouti rabbit, you will see “bandings” of different colors along the shaft of the hair, being blue, black, tan, fawn. The Agouti also has light tan coloring around the nostrils and at the back of the neck. The belly is cream.(http://rabbit.wikia.com/wiki/Agouti)

2, Chinchilla rabbit: soft, grey fur.

genetics 4 A five-week-old Chinchilla rabbit — A FIVE-WEEK-OLD CHINCHILLA RABBIT, image from the Internet

Chinchilla Rabbits originated in France and were bred to standard by M. J. Dybowski. They were introduced to the United States in 1919. (wikipedia)

3. Himalayan rabbit: white body with colored points, recognized colors are black, blue, chocolate and lilac.

A HIMALAYAN RABBIT, image from the Internet

red eyes; posed stretched out, body to be 3.5 head lengths. They are the ancestors of Californians, one of the most common meat rabbits.(wikipedia: Himalayan_rabbit)

4. Albino rabbit: completely white since it’s missing the melanin which determines the color of their skin, eyes, and fur.

genetics 4 albino rabbits — AN ALBINO RABBIT, image from the Internet

Not all white rabbits are albinos, so you’ll need to check their eyes. If their eyes are red or pink and their hair is totally white, they would be considered an albino. They are not rare.

An albino rabbit may not have the greatest eyesight due to their lack of eye pigment. Since their eyesight is not the best, they should be caged or kept inside since they may not be able to see predators.(http://www.ask.com/question/albino-rabbits)

Having seen so much about rabbits, hope you haven’t forgotten what we were doing before those cute bunnies. We were learning about examples of multiple alleles of one gene.

the human ABO blood group system.

(all form wikipedia: ABO blood group system:)

The ABO blood type is controlled by a single gene (the ABO gene) with three types of alleles inferred from classical genetics: i, I^A, and I^B. The gene encodes a glycosyltransferase— an enzyme that modifies the carbohydrate content of the red blood cell antigens.

The I^A allele gives type A, I^B gives type B, and i gives type O.

Both I^A and I^B are dominant over i, so only ii people have type O blood. Individuals with I^AI^A or I^Ai have type A blood, and individuals with I^BI^B or I^Bi have type B.

I^AI^B people have both phenotypes, because A and B express a special dominance relationship: codominance(we talked about it last class), which means that type A and B parents can have an AB child.

A type A and a type B couple can also have a type O child if they are both heterozygous (I^Bi,I^Ai)

Hope your mind is still clear!

NOTE: the concept of multiple alleles of one gene is totally different from multiple-gene inheritance.

A polygene, multiple factor, multiple gene inheritance, or quantitative gene is a group of, non-allelic, genes that together influence a phenotypic trait.

Example(1)

vocabulary

Diversity of chromosomes

Let’s begin with a relatively simple example.

When the situation gets a little bit more complicated:

A more complex situation:

The three examples above lead us to a new concept: Epistasis.

UV absorption

Thermodynamics of DNA

DNA topology

DNA superhelix

Thermodynamics of DNA