Genetics – AP Biology

Genetics [10] reproduction 3: Meiosis 2

Last section we gave a general introduction of meiosis in terms of chromosome behaviors.

In this section, we will deal with two other respects of meiosis. First, a specific description of meiosis in animals; second, we will mention a situation when meiosis goes wrong.

Meiosis in animals

is found only in ovaries (卵巢)and testes(曲细精管), and even in these tissues is restricted to cells that are destined to form gametes(the germline).

Despite the fact that the mechanisms of gametogenesis differ somewhat between organisms,the steps involved in gametogenesis in mammals are relatively similar.

In male gametogenesis (spermgenesis).

precursors of germ cells go through many rounds of mitotic divisions in order to maintain a pool of spermatogonia(plural of spermatogonium 精原细胞).↓

Spermatogonia subsequently differentiate into primary spermatocytes(based on what you learned in high school. guess what this word mean? : D ). It is in these cells that meiosis takes place.↓

After meiosis I, these cells are referred to as secondary spermatocytes. These are haploid. The products of the second meiotic division are spermatids. ↓

Spermatids differentiate into motile spermatozoa with rounded or elongate head and a long posterior flagellum.(The final activation of spermatozoa takes place after copulation/sexual intercourse)

Without cytoplasm and many subcelluar organelles, the sperm is light and fast (almost all its weight concentrated in its head, where stored the key of a potential life, nuclei. ).

In female mammals, the pattern of oogenesis is superficially similar.

Here oogonia(plural of oogonium, 卵原细胞) go through mitotic divisions before differentiating into primary oocytes. These then undergo meiosis.↓

Both daughter cells of the primary oocytes are haploid but differ greatly in size. The larger daughter cell is the secondary oozyte, the smaller the first polar body. The two cells remain attached. Both undergo a second meiotic division.↓

The secondary oocyte undergoes an unequal division producing a large ovum and a small secondary polar body. The first polar body divides into two secondary polar bodies.

Only the ovum, which contains almost all the cytoplasm, will transmit genes into the next generation.

The first meiotic division is only completed at ovulation(the discharge of a mature ovum from the ovary), and the second occurs after fertilization.

Little known: In human females, primary oocytes can be held in meiotic arrest for up to 45 years. This may be important in the increased frequency of aneuploid births observed in older mothers.

Production of aneuploid gametes

The major cause of anueploidy(the situation of having or being a chromosome number that is not an exact multiple of the usually haploid number) is aberrant chromosome behavior at meiosis. In other words, it’s the failure of chromosmes to segregate properly(known as nondisjunction)

At anaphase I, if two homologous chromosomes move to the same pole, first division nondisjunction occurs. In this case, of the 4 cells arsing from meiosis, two will be disomic(contain two copies of the chromosome) and two nullisomic (contain no copy of the chromosome.

At anaphase II, if the chromatids in a cell remain together, division nondisjunction occurs. The resulting tetrad will contain two normal cells, one nullisomic, and one disomic.

Aneuploidy also arises due to nondisjunction at an early mitosis in the embryo, resulting in two populations of cytogenetically different cells in the individual, which is known as a mosaic.

MOSAIC (GENETICS)"Heterochromia iridum and iridus" image from simple.wikipedia.org — MOSAIC (GENETICS)”Heterochromia iridum and iridus” image from simple.wikipedia.org

Mosaic is common in Turners syndrome.

↑Turner syndrome or Ullrich–Turner syndrome is a chromosomal abnormality in which all or part of one of the sex chromosomes is absent or has other abnormalities . In some cases, the chromosome is missing in some cells but not others, a condition referred to as mosaicism or “Turner mosaicism”.

Occurring in 1 in 2000– 1 in 5000 phenotypic females, the syndrome manifests itself in a number of ways. There are characteristic physical abnormalities which affect many but not all people with Turner syndrome, such as short stature,swelling, broad chest, low hairline, low-set ears, and webbed necks. Girls with Turner syndrome typically experience gonadal dysfunction (non-working ovaries), which results in amenorrhea (absence of menstrual cycle) and sterility. Concurrent health concerns may also be present, including congenital heart disease, hypothyroidism (reduced hormone secretion by the thyroid), diabetes, vision problems, hearing concerns, and many autoimmune diseases.Finally, a specific pattern of cognitive deficits is often observed, with particular difficulties in visuospatial, mathematical, and memory areas.

Turner syndrome is named after Henry Turner, the endocrinologist who first described it in 1938.（wikipedia）

Genetics [9] Reproduction 2: Meiosis

During the process of reducing the number of chromosomes by half, the combination of alleles are rearranged to give recombinant gametes. Two distinct processes are involved. These are independent assortment of chromosomes and crossing-over.

Meiosis involves twosuccessive divisions, resulting in producing four cells, each containing half the number of chromosomes of the mother cell. There is NO replication between the two divisions.

We call the two divisions meiosis I and meiosis II, as in Chinese 减数第一次分裂 and 减数第二次分裂. Here we will introduce more of meiosis than meets in high school textbooks.

Meiosis I

meiosis I is divided into prophase, metaphase, anaphase and telophase. Although they have the same names as the four phases in typical mitosis, behavior of chromosomes in these four phases in meiosis is very different from that in mitosis.

In prophase each chromosome pairs with its homolog (copy of the same chromosome inherited from the other parent). The paired chromosomes are called bivalents. Each pair is held together by chiasmata(plural of chiasma). The exchange of genetic material is known as crossing-over.

A chiasma (plural: chiasmata), in genetics, is thought to be the point where two homologous non-sisterchromatids exchange genetic material during chromosomal crossover during meiosis (sister chromatids also form chiasmata between each other, but because their genetic material is identical, it does not cause any change in the resulting daughter cells). (from wikipedia)

Prophase of meiosis is subdivided into five stages: leptotene, zygotene, pachytene, diplotene, and diakinesis.
In leptotene(literal translation:thin threads), the chromatin is seen to condense into very long thin strands, that appear tangled in the nucleus. As prophase proceeds chromosomes become shorter and thicker.
At zygotene(literal translation: yoked/linked threads), homologous chromosomes are seen as partially paired structures. They are still very elongated at this stage and chromosome pairs may overlap or interwine.
By patchytene(thick threads), pairing is complete, though it still isn’t possible identify clearly the individual chromatids in each bivalent.
As the homologous chromosomes begin to separate, transition from patchytene to diplotene(double threads) occurs.

This process begins at the centromeres and the bivalents are seen to be held together by chiasma.

The nuclear membrane and the nucleolus breaks down.

The four chromatids in each bivalent become identifiable and individual chiasma clearly to be identified.

Chromosomes carrying on condensing, the cell moves into diakinesis(moving apart), the final subdivision of prophase I.

The scheme below shows the five stages in prophase in a simple way:

At metaphase I the nuclear envelope breaks down, the bivalents lie across the equator of the cell with their centromeres attached to the microtbules←similar to the spindle in mitosis.

The dynamic action of the spindle causes one member of each homologous cell to move to the opposite poles of the cell.

↑WHY wouldn’t the action of the spindle tear apart the sister chromatids?

BECAUSE at metaphase the sister chromatids are held together by proteins called cohesions, which holds chiasmata in place and so holds the chromosomes together.

At anaphase I the cohesions in the chromosome arms are cut, allowing the homologs to separate.

In telophase I, two neclei form around the segregating chromosomes and a degree of chromosome decondensation is observed.

Meiosis II

The process of meiosis II closely resembles that of the typical mitosis.

In prophase II the chromosomes are seen to recondense within the two nuclei. At metaphase II, the nuclear membrane breaks down and chromosoms rearranged at the equator , the centromere splits and…At anaphase II and telophase II,the initial dipliod cell has divided into four…we already knew these in high school.

What we didn’t know in high school is that each of the four haploid cells has a different genotype. And in many instances the group of four haploid cells may remain together and is known as a tetrad.

SUMMARY OF MEIOSIS

Genetics [8]：reproduction 1

Reproduction takes place by one of two methods, asexual or sexual.

Asexual reproduction involves the production of a new individual(s) from cells or tissues of a pre-existing organism. This process is common in plants and in many microorganisms. It can involve simple binary fission(splitting into two) in unicelluar microbes or the production of specialized asexual spores(孢子).

NATURAL VEGETATIVE PROPAGATION. New plants grow from parts of the parent. (image from: leavingbio.net)

These processes may be exploited for commercial purposes as in the vegetative propagation of plants. More recently it has been possible to regenerate whole organisms from a single cell. This was first shown in carrots and frogs, but it has now been reported in mammals, and by implication, is possible in all mammals including humans.

Asexually reproduced organisms are genetically identical to the individual from which they were derived. A group of such genetically identical organisms is known as a clone.

Here I found an article at Buzzle , thinking it may help us learn more about animal cloning: http://www.buzzle.com/articles/animal-cloning/. Below is an excerpt of that article.

1, The Process of Animal Cloning
Initial attempts at artificially induced Animal Cloning were done using developing embryonic cells.

The DNA nucleus was extracted from an embryonic cell and implanted into an unfertilized egg, from which the existing nucleus had already been removed. The process of fertilization was simulated by giving an electric shock or by some chemical treatment method. The cells that developed from this artificially induced union were then implanted into host mothers.

The cloned animal that resulted had a genetic make-up identical to the genetic make-up of the original cell←the embryonic cell that contributes the DNA nucleus.

Since Dolly, of course, it is now possible to create clones from non-embryonic cells.

Now animal cloning can be done both for reproductive and non-reproductive or therapeutic purposes. In the second case, cloning is done to produce stem cells or other such cells that can be used for therapeutic purposes, for example, for healing or recreating damaged organs; the intention is not to duplicate the whole organism.

2. Ethics of Animal Cloning
While most scientists consider the process of animal cloning as a major break through and see many beneficial possibilities in it, many people are uncomfortable with the idea, considering it to be 'against nature' and ethically damning, particularly in the instance of cloning human beings.

The truth is that most of the general public are not aware of the exact details involved in cloning and as a result there are a lot of misconceptions about the entire matter.

In recent times, there have been a spurt of new laws banning or regulating cloning around the world. In some countries, animal cloning is allowed, but not human cloning. Some advocacy groups are seeking to ban therapeutic cloning, even if this could potentially save people from many debilitating illnesses.

3. Points against Animal Cloning
In a large percentage of cases, the cloning process fails in the course of pregnancy or some sort of birth defects occur, for example, as in a recent case, a calf born with two faces. Sometimes the defects manifest themselves later and kill the clone.

4. Points for Animal Cloning
On the favorable side with successful animal cloning - particularly cloning from an adult animal - you know exactly how your clone is going to turn out. This becomes especially useful when the whole intention behind cloning is to save a certain endangered species from becoming totally extinct.←for more info, please see http://www.buzzle.com/articles/cloning-extinct-animals.html

That this is possible was shown by cloning an Indian Gaur in 2001. The cloned Gaur, Noah, died of complications not related to the cloning procedure.

Speaking of saving extinct animals, I couldn’t help but think of Jurassic Park. Although in the movies looks like cloning extinct animals brings threat to humans, or maybe it truly would in reality, the idea of cloning them remains magically attractive to me. Especially, would the biodiversity allow, cloning those who became extinct because of our hunting.

What’s your idea?

Before I lead you off the topic, let’s go back and talk about Sexual reproduction, which differs from asexual reproduction, in that it involves fusion of cells (gametes←we knew in high school as配子), one derived form each parent, to form a zygote. The genetic processes involved in the production of gametes allow for some genetic changes in offspring.

The production of gametes is referred to as gametogenesis. This may be a complex process, involving sexual differentiation and the production of highly differentiated male and female gametes, or in lower eukaryotes identical cells may fuse–isogamy.

isogamy , in biology, a condition in which the sexual cells, or gametes, are of the same form and size and are usually indistinguishable from each other. Many algae and some fungi have isogamous gametes. In most sexual reproduction, as in mammals for example, the ovum is quite larger and of different appearance than the sperm cell. This condition is called anisogamy. (infoplease.com)

Whatever the biology of the process, one fact is obvious: gametogenesis must involve a halving of the chromosome number, otherwise each succeeding generation would have double the chromosome number of its parents.←That’s why, sexual reproduction is limited to species that are diploid or have a period of their life cycle in the diploid state.

Halving of chromosome numbers is achieved in a specialized form of cell division, meiosis(←we learned in high school as减数分裂), which is only observed in gametogenesis.

We will talk about meiosis more detailedly next section.

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。

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

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.

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.

Mendel’s Genetics[3]: Variations of the 3:1ratio

Variations of the 3:1 ratio

The simple 3-to-1 monohybrid ratio is not always observed in instances where only one gene is responsible for a particular phenotype.

A number of factors:

Partial or incomplete dominance

Complete dominance means the phenotype of first filial generation(heterozygous) is exactly identical to that of one of the parents(both homozygous). Partial or incomplete dominance means the first filial has phenotype somewhere between that of both parents.

For example, When two pure-bred snapdragons, with white and red petals respectively, cross, their first filial generation has pink petal rather than red or white.

In this case, the homozygous phenotypes are red, or white petals while heterozygous one is between white and red: pink petal.

Thus, it is conceivable that when it comes to the second filial generation, which was produced by the self fertilization of the heterozygous F1, F2 should have three different phenotypes, white, pink, and red. And we can also deduce the ratio of them is 1:2:1.

Codominance

Codominance is similar to incomplete dominance, but here the heterozygote displays both alleles(两种等位基因均被表达).

For example, in humans the MN blood group is controlled by a single gene.

In humans the main blood group systems are the ABO system, the Rh system and theMN system.

Only two alleles exist, M and N. Children whose father is an NN homozygote with N blood and whose mother is a MM homozygote with group M blood are MN heterozygotes and have group MN blood.Both phenotypes are identifiable in the hybrid. And the ratio also switches from 3:1 to 1:2:1.

Lethal alleles

Some alleles affect the viability of individuals that carry them.

In most cases the homozygous recessive does not survive but the heterozygotes may have a normal lifespan.

The best-known example of lethal alleles is the inheritance of yellow coat color in mice.

Yellow fur can arise in strain of mice with different colors, or instance, black. Yellow coat color is dominant to black coat. Mice with BB alleles are back, with BB^yare yellow, with B^yB^y alleles are supposed to be yellow as well, but B^yB^y alleles are lethal and any mice with this genotype die in utero(in the uterus : before birth).

SO it is conceivable that when two yellow mices are mated ratio of the different phenotypes of their first generation is 2 : 1, rather than 3 : 1 or 1 : 2 :1.

NOTE: The allele B^yis recessive in its relation to its effect on viability (only homozygous B^yB^ys die, while the heterozygotes survive ), but dominant in relation to coat color(heterozygotes present in yellow fur in stead of black fur.).

Other examples where alleles are lethal when homozygous but have a dominant effect when heterozygous, include :

tailless Manx cats

genetics — a manx cat, image from the Internet

a breed of domestic cat(Felis catus) originating on the Isle of Man, with a naturally occurring mutation that shortens the tail.

The Manx taillessness gene is dominant and highly penetrant; kittens from two Manx parents are generally born without any tail. Being homozygous for the taillessnees gene is lethal in utero.Thus, tailless cats can only be heterzygous. Because of the danger of having homozygous taillessness gene, breeders avoid breeding two entirely tailless Manx cats together.(wikipedia: Manx (cat))

short-legged Creeper chickens.

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(Annie: If none of the homozygous yellow mice can survive before birth, then where did all the heterozygous yellow mice come from in the first place???????)

Answer: Through mutation. The presence of one mutant allele alters development so as to produce characteristic changes to the animal, but when two of the mutant alleles are present, development is so aberrant as to cause death.

This may occur in utero as described above or resulted in shortened life expectancy as found in several examples in humans, such as Tay-Sachs disease, Huntington’s syndrome（亨丁顿舞蹈症） or sickle-cell anemia（镰刀形红血球病）. (from Instant Notes)

Mendel’s Genetics[2]: The monohybrid cross

Keywords:

Phenotype

Any character (trait) which can be shown to be inherited, such as eye color, leaf shape or an inherited disease, such a cystic fibrosis, is referred to as a phenotype.

Description: A fly may be described as having a red-eyed phenotype. A child may be described as displaying the cystic fibrosis phenotype.

Genotype

The pattern of genes that are responsible for a particular phenotype in a individual is referred to as genotype.

Dominance

In hybrids between two individuals displaying different phenotypes, only one phenotype may be observed. This phenotype is referred to as the dominant trait and the un-shown one the recessive.

For instance, if the wife has wide eyes while the husband has small eyes, and their little girl has wide eyes, then the wide eyes are dominant to small eyes.

Pure-breeding lines

Organisms which have been inbred for many generations in which a certain phenotype remain the same.Pedigree breeds of dogs or cats are commonplace examples of pure-breeding lines.

A puppy from two purebred dogs of the same breed, for example, will exhibit the traits of its parents, and not the traits of all breeds in the subject breed’s ancestry.

Homozygous: Individuals with two identical copies of a gene.

“True breeding (pure-breedind) organisms are always homozygous for the traits that are to be held constant.”

Heterozygous: Individuals with two different copies of the gene.
Alleles: The different variants of a gene.

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Mendel made a cross between two pure-breeding lines of pea plants, one of which had violet petals and the other white petals. The hybrids produced in this cross were referred to as the F1 (first filial) generation.

In Mendel’s experiment, the ratio of violet pedals and white ones in the second filial were very close to 3 to 1, which applied to the theoretic reasoning shown above.

He did many other experiments focusing on different types of genotypes of the pea plants and the results were shockingly similar. The hidden phenotype in the first filial reappeared in the second filial and the ratio of the dominant to the recessive phenotype were all close to 3 to 1.

The 3:1 ratio is referred to as the monohybrid ratio and is the basis for all patterns of inheritance in higher organisms.

One simple extension of the 3:1 phenotype ratio is a 1:1 ratio, produced when a heterozygous F1 individual is crossed to the homozygous-recessive parent. The process is known as testcross.

Testcross is useful in any condition when it is necessary to determine whether an individual is heterozygous or homozygous. Conceivable that if F2 all have dominant phenotype, then the tested parent is homozygous-dominant; if F2 have a 1:1 ratio of dominant and recessive phenotype, then the tested parent is heterozygous.