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Basic Genetics

For many keepers of gerbils, their coat colour genetics may not be of much interest to them or of much use, but for a breeder of gerbils it can be very useful to have a grasp of the basic genetics of the animal they have chosen to breed. This not only can save much time and tank space, and often many unwanted litters, but if you are after a certain coat colour, it will enable you to successfully predict the outcome of crosses so that your goals can be achieved with reasonable accuracy, and in a much shorter time period. It can often be a very disappointing experience for a beginning breeder if the two pretty coat colours they have just chosen to mate together go on to produces just Golden Agouti gerbils, but with a basic grasp of colour genetics this can be avoided. Saying this, breeding itself shouldn't ever be taken lightly, and breeding for coat colours should be secondary to good health and temperament. Good breeding includes good welfare and should also include the proper after care of the pups that have been produced and are now effectively in your care.

Cellular journey

To give you a greater understanding of how genetics work, we first need to look into the cell, and at genes, chromosomes and DNA, and to explain this we need to take a closer look at how a cell works in a gerbil's body. So let's move forward and go on a cellular journey into the working of a typical cell in the gerbil's inner ear.

 

Cell division

Now that we have explored cells and have a better understanding of chromosomes and the DNA within them, we now need to look at how a cell replicates itself, and more importantly how the mechanisms of cell division that occurs in sex cells can pass on genetic information from both parents to their offspring.

Cell division is the process by which cells multiply during the growth of tissues and organs. Cells first make an extra copy of their genetic material. One cell then splits into two new cells, each with its own set of genetic material and other cellular structures. Cell division can occur through mitosis or meiosis. In multi-cellular organisms such as humans and of course our Mongolian gerbil, it is the body (somatic) cells which undergo mitosis, while germ cells ( these are cells which are destined to become either sperm cells in males or ova in females) divide by a similar process that is known as meiosis.

Mitosis & Meiosis

 

Mitosis

This is the process of division of body cells in which each daughter cell receives the same amount of DNA as the parent cell. The cells produced here are identical to the original cell that has been divided. The chromosomes in the cells nucleus are duplicated to generate two daughter nuclei; this is then followed by a process called cytokinesis, which then divides the nuclei, cytoplasm, organelles and the cell membrane, into two separate daughter cells carrying a roughly equal share of all these cellular components.

Mitosis and cytokinesis are the defining processes of the mitotic phase of a cells life cycle. The mitotic phase itself is relatively short in the full cell cycle, and there are several other stages where a cell will grow, then duplicate its chromosomes, prepare for mitosis and then finally divide. Each phase has its own particular name and can be seen in extreme detail in the photographs in the gallery below.

Errors In Mitosis

Mitosis in itself is a traumatic period for a cell, and although extremely rare, this process can go wrong. Errors in mitosis can be potentially dangerous to an organism because any future replications from an error in a parent cell will then carry the same disorder. The effects from an abnormal cell can all depend on the specific nature of the error and may range from being benign to having a noticeable effect, through to cell mutations that can lead to cancer. In many instances an error in cell mitosis will cause apoptosis, which will kill the cell. "Apoptosis" is a programmed cell death and can occur for several reasons such as when the cell is damaged beyond repair, or infected with a virus, etc, and the decision for apoptosis can come from the cell itself, surrounding tissue and even from another cell that is part of the bodies immune system. In these instances apoptosis is a beneficial process, however if apoptosis cannot occur due to a mutation or a biochemical inhibition, the cell itself will continue to divide and this process can develop into a tumour.

Mitosis gallery

 

Meiosis

This is a special form of cell division in which each daughter cell receives half the amount of DNA as the parent cell. Meiosis occurs during the formation of egg and sperm cells in mammals. During meiosis all the hereditary information stored in the DNA on chromosomes in a diploid germ cell undergoes DNA replication which is followed by two rounds of division, the net result being the formation of haploid cells known as gametes. These haploid cells can then fuse with other haploid cells of the opposite sex during fertilization to create a new diploid cell or zygote (a cell which is a result of fertilization) the zygote then undergoes mitotic cell division to eventually form an embryo.

A diploid cell is simply a cell that contains genetic information from both parents. In humans most cells are diploid; they carry one set of chromosomes from each parent. A haploid cell is the sex cells (ova and sperm) and refers to their chromosome content which only has one copy of each chromosome, so have only half the number of chromosomes that are found in other cells of the body.

Meiosis ensures that each zygote produced will have a unique set of genetic blueprints encoded in its DNA, and the process of meiosis and sexual reproduction ensures genetic variation.

The process of meiosis uses many of the same biochemical mechanisms that are used during mitosis, but meiosis has several unique features. The Mongolian gerbil also has a unique form of meiosis that is shared with marsupials and some insect species, and that is the sex chromosomes that pair and segregate during the meiosis of male gerbils do so without undergoing meiotic recombination. We know that meiosis is a special kind of cell division that leads to the formation of gametes, and that the number of chromosomes has to be halved in the daughter cells, and to ensure this is done properly most organisms use a strategy where during the first of the two meiotic divisions, homologous chromosomes will associate in pairs, and then undergo a reciprocal genetic interchange, which is known as meiotic recombination, and this ensures that these homologous chromosomes remain very tightly knitted until they eventually segregate. In male gerbils though there are several proteins that are reorganised to make sure that sex chromosomes are tightly knitted together until they eventually segregate, without them having to undergo meiotic recombination.

Errors In Meiosis

In Mongolian gerbils, germ cell loss (apoptosis) helps regulate the amount of sperm produced, which occurs mainly during meiosis. This process ensures that most often defective cells and also cells that carry DNA mutations are eliminated. Studies on male Mongolian gerbils have shown that around 30% of germ cell loss occurs during meiosis.

Mendel's Laws

To understand the concept of how certain coat colours are passed on from generation to generation, and how some colours may skip a generation, it is worth understanding how traits are inherited, and by what laws these traits adhere to.

Mendelian traits

These are traits that are controlled by a single locus and will show a simple and predictable pattern of inheritance. A locus (Plural: loci) is a specific site or position on a chromosome that is occupied by a specific gene.  In our case with gerbils, a mutation in a single coat colour gene can cause the colour to be inherited according to Mendel's laws.

Mendelian Inheritance

These laws were derived by Gregor Mendel, a 19th century Austrian monk, when conducting his experiments with pea plants and their hybrids. In the years between 1856 and 1863 he grew and tested somewhere in the region of 28,000 plants. These experiments resulted in two basic generalisations which were later to become known as Mendel's laws of heredity, which were described in his essay on plant hybridization. Mendel's results were largely left neglected until much later when they were rediscovered around 1900, and were initially very controversial. In 1915 they were integrated with the chromosome theory of inheritance by Thomas Hunt Morgan, an American geneticist and embryologist and they went on to become the core of classical genetics.

Mendel's first law

This is essentially in four parts and they are known as the laws of segregation.

1) Alternative versions of genes account for variations in inherited characteristics.

This is the idea of alleles. Alleles are viable pieces of DNA coding that occupy a point on a given locus, and are usually the sequences that code for a gene. In diploid organisms such as mammals, they have two copies of each chromosome, and two alleles make up each individuals genotype. In our case with gerbils, it is the genes that control fur colour that we are interested in, and there may be several different versions, or alleles of these genes. The resulting colour of the fur of an individual gerbil will all depend on which two alleles it possesses for the gene and how the two alleles interact.

2) For each characteristic, an organism will inherit two alleles, one from each parent.

This means that when somatic cells (the cells of the body) are produced from these two alleles, that one allele will come from the mother, and the other from the father. These alleles can be the same, true breeding or homozygous, for example in gerbils, 'AA' will be homozygous, or these alleles can be mixed such as 'Aa' for hybrids or heterozygous individuals.

Zygosity

In genetics zygosity refers to the genetic condition of the zygote, and is referring to the similarity or dissimilarity of DNA between similar chromosomes at a specific allelic position or gene.

Homozygous

This means that the alleles at the same locus on a pair of similar chromosomes that are paired during meiosis are identical. It also refers to a genotype that consists of two identical alleles of a gene for a certain trait. So for example, in gerbils an individual could be either homozygous dominant 'AA' or homozygous recessive 'aa'.

Both 'AA' and 'aa' gerbils are true breeding and are known as homozygous.  This means they only have one type of gene at that locus, so this gene is the only one that can be inherited by their offspring. To demonstrate this we can cross two homozygous 'AA' Golden agouti gerbils together. This simple breeding demo below will show us the outcome of such a cross.

 

 

In gerbil offspring we also know that each pup receives one copy of each gene from both its mother and father at random. Now if two black parents have offspring they only have the non-agouti or black mutation at the A locus to pass on, the offspring can only receive 'a' from both parents, so they can only be black. We can see this working in this simple breeding demonstration with two 'aa' agouti gerbils.

 

 

Heterozygous

This means that the genotype consists of two different versions of the alleles of a gene for a particular trait. For example in gerbils, one of the copies of the gene may be the normal version, the other the mutation (Aa) Individuals who are heterozygous for a trait are referred to as heterozygotes.

'Aa' type gerbils are referred to as being heterozygous, which means they have two different types of genes at that particular locus, one being dominant or the normal version of the gene, the other is recessive and is the mutation. This type of genetic combination would occur if we mated two gerbils that had differing genes at the same locus.

To demonstrate this simply, if we use the two gerbil colours Golden Agouti and Black and breed them together, the offspring will receive one of their genes from each parent, so although the offspring may all look the same and be Golden Agouti, they will have different genes to their homozygous agouti parents. We can see this in the demo below.

 

 

Hemizygous

This means that there is only a single copy of the gene in an otherwise diploid organism. For example, in gerbils we can see this in the sex chromosomes in a male. Since there is only one copy of either the X or Y chromosome in the germ cell, the term homozygous or heterozygous are inappropriate.

3) If the two alleles differ, then A) the allele that encodes the dominant trait is fully expressed, and B) the allele encoding for the recessive trait will be masked by the dominant trait and will have no noticeable effect on the organism's appearance.

This essentially means that only the dominant trait is seen in the phenotype of the animal. This effect then allows the recessive traits, or the recessive alleles, to be passed down to the offspring even if they are not expressed in the first generation (F1 or filial generation)

Dominant and recessive genes

Each gerbil inherits a copy of each chromosome from its mother and a copy from its father. The parents therefore pass on one of each pair of these genes to their offspring (in our case the genes that create the characteristics of the coat colour).  As we now know, at each locus there may also exist alternative genes, these alternative genes we also know are named alleles. The individual loci and genes that give gerbils their coat colours are denoted letters to indicate a certain characteristic. Dominant characteristics are given a capital letter and recessive characteristics are allocated a lower case letter.

We also now know that each gerbil has two copies of each gene. In the above cases the gene that controls agouti patterning is given the symbol 'A', and the recessive mutation that gives us black, or non-agouti is given 'a'.

A- Agouti

a- non-agouti (Black)

So our gerbil at the A locus can either be 'AA' (homozygous dominant), 'Aa' (heterozygous) or 'aa' (homozygous recessive). When it has either 'AA' or 'Aa' the gene still has the functioning protein to create the banding in the gerbils coat, but if the gerbil is aa the protein is non functional, so our gerbil will be black and will not have the agouti pattern. This demonstrates how simple dominance works.

Note that in the simple demonstrations shown we will only be dealing with four offspring. This is mainly to show that when dealing with simple inheritance of a single characteristic that the offspring will have a probability of inheriting the genes in the ratios that are given. However in true breeding terms, do not expect the colours to appear like this in every litter as this is also governed by the rules of probability, and like the flip of a coin, where you can never be sure of which side it that it lands on, this also holds true for each gerbil colour that is produced in a litter.

However it should be noted here that not every trait is simply dominant or recessive, and some gene traits exist in organisms which are either incompletely dominant or they can also be co-dominant.

4) The two alleles for each characteristic will segregate during gamete production

This means that each gamete will contain just one allele for each gene and this will allow the alleles from the mother and father to be combined in their offspring, and this ensures natural variation. It should be noted here that it is often thought that it is the gene itself that is dominant, recessive, and incompletely dominant or co-dominant, where in actual fact it is the trait or the gene product that the particular allele encodes that is either dominant or recessive, etc.

Before we venture any further it's probably time to introduce a tool that enables us to track and understand the gene interactions of these crosses that we are going to make. It is quite straightforward and easy to use, and is known as the Punnett square.

The Punnett square and the probability of inheritance

The Punnett square is a predictive tool that is still used today which helps determine the mathematical probability of offspring in crosses having a particular genotype. This concept was designed by Reginald Punnett, a British geneticist who helped introduce genetics to the public with his published work Mendelism in 1905. He also co-founded, along with William Bateson the Journal of genetics, the scientific journal of genetics and evolution in 1910.

The diagram helps determine the outcomes of crosses by graphically comparing all the possible combination of alleles from the mother with those of the father. To use this method, all you have to do is to create a table, where at the top you write the genotype of one parent, then down the side the genotype of the other parent. You then record for each of the parents, all the possible combinations of their genes that the animal or plant can pass on. So using our purebred cross for an example, a gerbil that is 'AA' can pass just 'A' to its offspring and a gerbil that is 'aa' can only pass on 'a' to its offspring, but both have two copies of the gene so it is noted down twice as it helps us define the ratios and probabilities.

As you can see by the example below, you have four boxes where you can fill in all the genetic combinations, and to complete the table you cross reference the relevant genes from both parents. So in our example in the top left hand box we will enter 'A' from the mother, and 'a' from the father which gives us the combination 'Aa'. We know that the dominant gene masks the effect of the recessive one, so this produces a golden agouti, and we can also include this information as well. We can carry on and fill in the next box in the top right hand corner and write 'Aa', which we again know is Golden Agouti, so can write this in too, etc. we then carry on cross referencing for the two lower boxes.

 

 

Monohybrid cross

A monohybrid cross typically compares just one trait and is a type of cross between two individuals who are identically heterozygous at one particular locus, for example if we again stick to the Agouti locus in gerbils, it would be a cross that is Aa X Aa, and monohybrid inheritance, is the inheritance of a single characteristic, and the different types of the characteristic are controlled by the differing alleles of the same gene.

Filials

When we are examining diagrams that show us the relationships between the families over the generations, you may see them being labeled as P1, then F1, F2, etc. Quite simply, P1 means the parents, or the parent generation, and then each successive generation is labeled with the F prefix. F is shorthand for filial which literally means "having or assuming the relation of a child or offspring" When Mendel conducted his pea experiment he noticed the temporary loss of a variation, in the first generation (F1) of offspring when breeding two purebred varieties together. However in the following generation (F2) the variety appeared again in the 3:1 ratio. Two of the offspring would be heterozygous, one would be homozygous dominant, and the other would be homozygous recessive, this being the purebred variety that disappeared in the F1 generation. We can see the same effect happening when we examine a cross at the Agouti locus with gerbils.

In the case of our Agouti locus in gerbils we know that there are two alleles, one for agouti or 'A' which is dominant, and the other for non-agouti or black, which is 'a'. So for example if we crossed two pure breeding strains of this gene, 'AA' for golden agouti with 'aa' which is black, we know that 'A' is dominant to 'a', so this will mask the black characteristic, so all the offspring in the F1 generation will be Golden agouti, but they will also be heterozygous, that being 'Aa'. For such monohybrid crosses, the parent genotypes are homozygous, and their offspring, or the F1 generation will all be heterozygous. We saw this earlier in our first example using the Punnett square.

So what would happen if we mated two of our heterozygous golden agoutis together?

 

 

Again we can plot this out using the Punnett Square below;

 

 

As you can see we have a ratio of three golden agoutis to one black gerbil, or a 3:1 phenotypic ratio, but we also have a 1:2:1 genotypic ratio in our example above. The golden agoutis are a combination of both heterozygous and homozygous individuals. While it holds true that this type of cross will average out in a 3:1 ratio over time, we cannot expect the colours to appear like this in every litter, because as we mentioned earlier, the colours appearing are also governed by the rules of probability.

In general, monohybrid crosses are used to determine the F2 generation from a pair of homozygous grandparents, usually one being dominant, the other recessive. The pairing of these F1 offspring gives us the F2 generation, with a 75% chance for the dominant phenotype to appear and a 25% chance for the recessive phenotype to appear.

Gerbil Mutations

If we take a look at the known mutations in the gerbil, at the time of writing this there are nine known mutations that change the coat colour, two responsible for patterning,and two that affect the coat structure.  Since its introduction into captivity in 1935 the majority are inherited recessively, bar three, these are Dominant Spotting, Semi-Dominant Lethal Spotting (patterning genes) and Rexoid.   A successful coat mutation is an exceptionally rare event in many species and occurs when their DNA gets modified in some way. Alterations in cells happen all the time, however these abnormal cells don't usually prosper. DNA repair mends most changes before they can become permanent mutations, and many organisms have specific mechanisms for eliminating these abnormal cells. Sometimes, if this alteration occurs early on in an animal's development, such as in the sperm, ova or zygote, the abnormal cell may succeed and have a chance of survival.

When considering a mutation that affects just the hair colouring in an animal, and not one that can also cause a problem elsewhere in the animal's development, the odds will increase as to whether the chances of this altered gene will survive. In certain instances a mutation that affects the hair or coat colour, may also go on to cause detrimental effects to the normal functioning of the organism. Most mutated genes are also recessive in nature, so the individual with this mutation still has to go on to reproduce successfully. If this has been accomplished, two of the descendents will have to reproduce again before you see the mutation surface once more. Over a relatively long time period these mutated genes will then have to be built up in the population, and that's all providing whether the mutation is actually beneficial for the species.

You can now begin to see how such a rare occurrence a successful mutation really is, and appreciate how high the odds are at a new mutation eventually succeeding!

So what exactly is a mutation?

Now that we've been on a cellular journey into a gerbil's inner ear, we know that every single cell in a gerbil's body contains a nucleus. The nucleus itself contains a number of chromosomes containing DNA. If we look closely along these chromosomes, we see that coded within their DNA are a series of genes. These genes create specific proteins. The proteins that are created by genes have very specific functions, which are very wide ranging. There are many examples of this, and we have seen that sometimes they act as a catalyst to help another process to take place within the body, or they can just as easily be used to create something, such as the protein collagen, which helps make body tissues both strong and flexible, or keratin which is responsible for growing hair and nails, and let's not forget about pigment enzymes which give rise to our gerbil's eye and fur colours. In essence, this means that the genes that lie within the chromosomes are responsible for a whole range of differing processes that take place within an organism's body, and the processes rely on groups of genes to produce specific proteins to enable them to take place, either producing hormones, body tissues or even a body characteristic. In the case of the gerbil, the characteristic we are interested in is their hair, or more specifically, their coat colour and coat structure.

The proteins that are produced by the coding of DNA are very specific in nature, so if the sequence of their DNA is altered, even slightly, this can affect the proteins function by either partially stopping, stopping altogether or even completely altering the protein that is produced. This change in the DNA is referred to as a "mutation".

For an organism to function properly, each individual cell depends on differing proteins to function in the right place and at the right time. If a mutation occurs in a protein that plays a critical role in the body, a medical condition will result, which is known as a genetic disorder. However most mutations have little impact on health, for example, they may only alter a genes DNA base sequence (see the flash movie here to learn about bases) but will not alter the protein function that is made by a gene. In most cases, as mentioned earlier, mutations that could represent a genetic disorder are repaired by the DNA repair system of a cell. Individual cells have several pathways in which enzymes recognise and repair DNA, and because DNA itself is subject to damage and mutation in many ways, the whole process of DNA repair is an important factor in protecting the body from disease.

In hereditary diseases, we are dealing with a mutation that is present in a germ cell, which in turn will give rise to offspring carrying the mutation in all of its cells. However a mutation occurring in a somatic cell of an organism will cause this mutation to be present in all the descendents of this cell, and certain mutations can cause the cell to become malignant, which will then gives rise to cancers.

It has also been shown that mutation rates will vary from species to species, and evolutionary biologists theorise that higher mutation rates are beneficial to a species in certain situations, because they allow the organism to adapt and evolve  quickly to an ever changing environment. We can see this with bacteria that are repeatedly exposed to antibiotics, and the selection of resistant mutants can result in strains of bacteria that have a higher mutation rate than the original population. In science these are referred to as mutator strains.

In all wild populations of animals there will always be some forms of slight variations in their DNA, and animals that are radically different from the norm may not fair so well for obvious reasons. However some mutations or variations in the DNA can have advantages that benefit the species long term. Mutations create variations in the gene pool, and natural selection eradicates the less favourable mutations from the gene pool. The favourable types of mutations accumulate in the gene pool, which over time result in evolutionary change within the species. Imagine a butterfly species that through ultraviolet radiation from the sun, produced a change of wing colour in its offspring. Now in most instances this wouldn't do the species any good, and there was certainly no purpose for it at the molecular level, but if this change of colour made it better for the butterfly to evade predators, and was also effective camouflage for the butterfly, then this mutation increases the survival rate.  Through successful reproduction, this mutation will then be passed on to its offspring. Over time the number of butterflies with this mutation will form a large percentage of the original species population.

Diseases or parasites which take advantage of an animal's specific protein may not fair so well if that protein had been altered due to a mutation, and due to this occurring they maybe resistant to the disease or the parasite. These variations in DNA can benefit the species over time. An extreme example of this in humans would be the recessive mutation that causes sickle cell disease. This disease is common in sub-Saharan Africa, where malaria occurs frequently, however it can still occur in other ethnic populations. As a result of this, those with one allele of the sickle cell disease are resistant to malaria since their red blood cells are not affected by the parasites. Those with two alleles, although resistant to malaria, have the accompanying sickle cell disease which is extremely debilitatating and considerably reduces their lifespan. This mutated allele has incomplete dominance, which means that even individuals who have just one mutated allele will still retain immunity to the disease. Although the positive side effect of this mutation is beneficial, and Mendelian laws makes it possible for some people to carry the advantages without the disadvantages of full blown sickle cell anaemia, there would need to be further mutations to solve the problem of the full blown disease in the population.

A very small percentage of all mutations though do have a very positive effect, and these lead to new versions of proteins that help the organism to adapt and survive in a changing environment. In humans we have an example of this with a specific 32 base pair deletion CCR5 (CCR5-Δ 32) which results in HIV resistance to homozygotes and delays the onset of AIDS in heterozygotes. The CCR5 mutation is relatively common to people of European descent. There exists a theory that maybe a reason for the relatively high frequency of CCR5-Δ 32 in the European population is that it gave resistance to the bubonic plague in mid-14th century Europe. People who had this mutation survived the plague, so the frequency of the mutation increased in the population. This could also explain why this mutation isn't present in African populations, as bubonic plague never reached there. Other theories say that it was selective pressure placed on the mutation by smallpox and not bubonic plague. Either way, it shows how such a specific mutation becomes beneficial to a population over time.

Mendel's second law

The law of Independent Assortment

This is the inheritance law which states that the inheritance pattern of one trait will not affect the inheritance pattern of another trait. In Mendel's experiments when he crossed one trait, they always resulted in a 3:1 ratio between the dominant and recessive phenotypes like we saw in our monohybrid crosses, however these ratios altered in his experiments when he mixed two traits together. These types of crosses are known as dihybrid crosses.

Dihybrid cross

Up to now we have dealt with just a singular characteristic, in our case, that of the non-agouti mutation, to help explain the laws of simple inheritance. However we know that although these breeding principles hold true, we also know that there are several other mutations at differing loci that deal with other factors that can effect the overall colour and make things a little complicated, so how would we deal with certain matings that pass on several colour characteristics at different loci, and not just one? Well this is where the Punnett square comes into its own, as this method allows us to manually calculate all the various genetic combination of alleles for any gerbil cross.

In addition to the non-Agouti mutation, there exist several other mutations that are capable of changing the gerbils overall colour. The one we will look at to demonstrate a dihybrid cross will be the pink-eyed dilution mutation. This mutation, like non-Agouti is recessive in nature, and is allocated the symbol 'p'. The mutation when homozygous, will turn a normal agouti's eye colour to red, and dilutes the black pigment in the coat so that it is a rich golden colour, the coat variety being known as the Argente Golden. In a self coat, one with the non-agouti mutation, it will change the coat to a lead grey, and it will dilute the eyes to red, this coat colour variety is known as the Lilac.

If we look at gerbils that will have all the possible combinations of these genes of both the A locus and the P locus, we can see that there are several combinations that make gerbils either Agouti, Argente Golden, Black or Lilac.

Firstly for Golden Agouti there would be...

AAPP AaPP AAPp AaPp

For Blacks there would be...

aaPP aaPp

For the Argente Golden there would be...

AApp Aapp

And finally our Lilac variety would be...

aapp

 As you can see, there are four possible genetic combinations of Golden Agouti from a heterozygous 'AaPp' X 'AaPp' mating. When we track these genotypes using the Punnet square we can also work out the probabilities for each genotype of Golden Agouti produced by this cross, and although they will look Golden Agouti, eight out of nine of them will be heterozygous and carry recessive genes, and almost half of them will carry both 'a' and 'p'. The same can be calculated for all the various combinations and is shown in the table on the breeding demonstration.

So firstly let's create our F1 hybrid from homozygous dominant and homozygous recessive gerbils at the A and P locus

 

 

Now a dihybrid cross is one where the two individuals that are identically heterozygous at two loci, and we are tracking the two genes from each parent to their offspring. Previously where our gerbil was 'Aa' it could only pass on either 'A' or 'a' to it's offspring. This time the Gerbil that is heterozygous would be 'AaPp', so can pass on 'AP', 'Ap', 'aP' and 'ap'. Using our punnet square we can see how these genotypes interact to produce phenotypes in a 9:3:3:1 ratio, this ratio being typical when two gerbils that are both carrying the same two recessive genes are mated together. Even so, these ratios only represent the chances of each of the offspring being a particular colour, and while over a large number of offspring we could expect one in sixteen being a Lilac coat colour, you cannot guarantee this.

 

 

The rules of meiosis as they apply to the dihybrid cross are shown clearly both in Mendel's laws of segregation and laws of independent assortment. For the genes on the separate chromosomes, each allele pair shows independent segregation, and the resulting F1 generation produces heterozygous individuals for the two gene traits, where as the second or F2 generation, which occurs by crossing the members of the F1 generation go on to produce a phenotypical ratio of 9:3:3:1. It is interesting to note that if we look closely at one trait at a time, the two different genes involved are still independently inherited in the usual manner, i.e. a 3:1 ratio.

Mendel concluded from his experiments with dihybrid crosses that different traits are inherited independently of each other. This is the general rule of independent assortment, but today's scientists know that this is only true if the genes involved that effect the phenotype are found on different chromosomes. The exceptions to independent assortment occur when genes appear close to one another on the same chromosome and they are usually inherited as a single unit. This is known as gene linkage and was discovered by the British geneticists Reginald Punnett and William Bateson, shortly after the rediscovery of Mendel's laws.

Test cross or Back cross

Now we have looked at some very simple breeding strategies and tracked the genes both on a single locus and at two loci, we are left with crossing a heterozygous individual (F1 hybrid) back to a homozygous individual.

The back cross or test cross were simple methods devised by Mendel to verify the genotype of the F1 hybrid, and can be used for checking the correctness of Mendel's law of segregation (using a monohybrid test cross) and the law of independent assortment (using a dihybrid test cross)

Monohybrid test cross

In our monohybrid cross of 'AA' x 'aa' all the F1 generation were 'Aa' (heterozygous Golden Agouti), so let's see what would happen when this F1 is test crossed with the homozygous recessive parent ('aa' Black).

In this cross we are aiming to verify two things. 1) To determine the genotype of the F1 Golden Agouti, and 2) to check the correctness of the law of segregation.

So if we backcross our F1 Golden Agouti with the homozygous recessive Black parent and examine the offspring, we know the recessive Black with 'aa' genotype will produce only one type of gamete, i.e. all with 'a' only, However regarding the F1 Golden Agouti, there could be two possibilities:

A) If the F1 Golden Agouti is homozygous ('AA') it would produce only one type of gametes, i.e, they would all be 'A', and as a result of this, the progeny of the test cross would all be Golden Agouti. 'AA'x'aa' = 'Aa' Golden Agouti

B) If the Golden Agouti is heterozygous with 'Aa' genotype and if Mendel's law of segregation is correct, then the F1 should produce two types of gametes, both 'A' and 'a' in equal proportions. So our test cross progeny should be 50% Golden Agouti and 50% Black or a 1:1 ratio.

 

 

As you can see from our breeding demo, the actual test cross agrees with the theoretical expectations and proves that the F1 Golden Agouti is a heterozygous dominant (monohybrid) with 'Aa' genotype and that the alleles segregate during gamete formation.

Dihybrid test cross

In our dihybrid cross of Golden Agouti ('AAPP') x Lilac ('aapp') the resulting F1 dihybrid is a double heterozygous Golden Agouti with 'AaPp' genotype. So we test cross this gerbil with the homozygous recessive parent Lilac (aapp). We are aiming to test the correctness of Mendel's law of independent assortment. If this principle holds true, the 'AaPp' dihybrid should produce four types of gametes: 'AP', 'Ap', 'aP' and 'ap' in equal proportions. The recessive Lilac Parent ('aapp') should only produce one type of gametes, that being 'ap'. So it is expected that the maximum possible chance combinations between these gametes should produce four kinds of phenotypes in a 1:1:1:1 ratio.

When Punnet squares deviate from the known phenotypic ratios

The phenotypic ratios of 3:1 and 9:3:3:1 are theoretical predictions based on Mendel's laws of inheritance, but deviations from these expected ratios occur in certain genetic scenarios, and some of these are applicable to crosses involving gerbil coat colours. Below are some examples that cause deviations from the expected ratios.

  • The alleles in question are physically linked on the same chromosome.
  • The survival rates of different genotypes are not the same. For example if a combination of alleles occurs that are lethal and the affected offspring die in utero.
  • The alleles are incompletely dominant or codominant.
  • There are genetic interactions between alleles of different genes (epistasis).
  • One of the parents lacks a copy of the gene. For example, in humans the male has only one X chromosome which is from his mother, so only the maternal alleles have an effect on the organism These are called sex linked genes.
  • The trait concerned is inherited on genetic material from only one parent. For example mitochondrial DNA is only inherited from the mother.
  • The alleles are imprinted. Normally in diploid organisms somatic cells possess two copies of the genome. Every autosomal or non-sex chromosome is represented by two alleles that are inherited from each parent at fertilization. In the vast majority of these autosomal genes, expression occurs from both of these alleles simultaneously. However a small proportion of genes are imprinted, which means that the expression of the gene occurs from just one allele, and is also dependent on its parental origin.

Of course there are other instances such as polygenic traits, multiple allele series, modifying and regulator genes, incomplete penetrance, sex related genetic effects, pleotropy, stuttering alleles and of course environmental influences which can all alter simple Mendelian inheritance, and as scientists learn more about the inheritance patterns for differing traits, it is becoming clear that genes that follow the simple rules of dominance seem to be becoming increasingly rare! It wouldn't be suprising in the future that scientists will discover many other exceptions to the rules of Mendelian genetics.

In 2005 there was an amazing example of this reported in a type of cress plant. These plants seemed to be able to overwrite the genetic make-up inherited from their parents! They were found to be able to revert back to the DNA sequences of their grandparents including genetic information that was lost in the intervening generations. Researchers on the subject have theorized that since the DNA sequences weren't present in the parents, that there could be some form of "template-directed process that makes use of an ancestral RNA-sequence cache".

Genome-wide Non-Mendelian Inheritance of Extra-genomic Information in Arabidopsis, Nature, Vol. 434, No 7032, March 24, 2005

If we take one of the above examples, that where the combinations of alleles are lethal, and the affected offspring die in utero, we can then show how the ratio changes when this occurs using Punnett squares.

Dominant spotting, like its name suggests is a dominant gene, and is usually best dealt with separately from other genes as it works as a pattern that is overlaid onto any existing gerbil colour, and variations in the patterning, like collared, mottled, variegated, are thought to be achieved by modifying genes that work on the spotting gene to achieve this effect. When using shorthand notation here, the wild- type gene is described as '+' as this gene hasn't been allocated a defining symbol in any published literature. Gerbils that are unspotted have two copies of the wild-type gene so are allocated the symbol '++'. Spotted gerbil are allocated the symbol 'Sp', and gerbils are either '++' or 'Sp+' because the 'SpSp' combination is pre-natal lethal and pups with two copies of the Sp gene are reabsorbed in the womb.

We can show how the spotting gene interacts when bred in the following Punnett square demos below...

 

 

This 2:1 ratio in the last example is what you would expect from a lethal gene (in the case of dominant spotting it is deemed pre-natal lethal), The normal 3:1 ratio of a dominant gene isn't seen and is replaced by the 2:1 ratio. Many people have misinterpreted these results and chose not two breed two spotted gerbils together believing that a spotted x spotted cross results in small litters because of the death of the homozygotes. However the truth of the matter is that the homozygotic embryos that are reabsorbed in the womb are simply replaced by viable embryos, and this is why we do not see small litters when mating 'Sp' to 'Sp' in gerbils. Their litter sizes remain normal and comparable to their unspotted counterparts.

Separator Gerbils

If we have a gerbil of unknown ancestry and wish to know its genetic code, there are several ways we could go about this. If for example we take our Golden Agouti gerbil again and cross it to another Golden Agouti, and then find that in the offspring that a quarter of them had the black coat colour, we can quickly conclude that both the parents carried the non-agouti mutation and were therefore 'Aa' at the Agouti locus. However if it were just our Golden Agouti that was 'Aa' and the other Golden Agouti was 'AA', then this type of cross wouldn't help us out at all. The most obvious way to find out if our Golden Agouti was carrying the non-agouti mutation would be to breed it to a Black gerbil. This would ensure us that the Black parent only had 'a' to pass on to its offspring, so half of the pups that may inherit 'a' from the Golden Agouti would then be Black themselves.

So, with careful crosses, we can quickly discover what recessive genes our Golden Agouti with unknown ancestry has. If we logically take this a step further and attempt to cover two gene loci, we could cross our Golden Agouti with a Lilac. We know that our Lilac is 'aapp' and has two copies of the mutations at both the A and the P locus, so we could expect four possible outcomes in our offspring. These outcomes could be either:

  • Only golden Agouti gerbils appeared in the litters: this tells us that our Golden Agouti must be 'AAPP', and wasn't carrying either mutation.
  • A mixture of Golden Agouti and Blacks appeared: This tells us that our Golden Agouti was carrying the non-agouti mutation, but not the pink-eyed dilute mutation. So our Golden Agouti must be 'AaPP'
  • A mixture of Golden Agouti and Argente Goldens appeared: This tells us that although our gerbil wasn't carrying the non-agouti mutation, it was carrying the pink-eyed dilute mutation. So our Golden Agouti is therefore 'AAPp'
  • A mixture of Golden Agouti, Argente Golden, Black and Lilac pups appeared: This then tells us that our Golden Agouti gerbil was carrying both the non-agouti mutation and the pink-eyed dilution mutation. So our Golden Agouti is 'AaPp'.

Over the course of several litters we would expect the ratios of Golden Agouti to the various colour mutants to come out as approximately 1:1. This is because in our previous monohybrid and dihybrid crosses we involved both dominant and recessive genes in both of the parent gerbils, and these dominant genes result in the recessive mutations not being expressed in the offspring. As a result the odds are stacked in favour of the dominant traits being expressed, so our ratios change. Here we observe ratios of 1:1 because we have chosen our Lilac carefully (As we did in our backcross/testcross example) and it only has the recessive genes at both the A and P locus.

In this mating we are only concerned in which genes are being passed on to the pups, and essentially it was only our Golden Agouti of uncertain ancestry that we were testing. If we take for example that our Golden Agouti was indeed 'AaPp', there were four possible gene sets that could have been passed on, and all would arise with equal probability, these sets being 'AP' 'Ap' 'aP' and 'ap'. These genes when combined with the Lilacs genetic contribution of 'ap', must then give us Golden Agoutis being 'AaPp', Blacks being 'aaPp', Argente Goldens being 'Aapp', and of course Lilacs 'aapp'. If however our Golden Agouti was only carrying just one of the recessive genes, and was for example 'AAPp', then in the scenario it could only pass on two gene combinations, those being 'AP' and 'Ap' and would give us approximately a 1:1 ratio of Golden Agouti to Argente Golden pups. Even though the Lilac gerbil was contributing 'a' to the offspring, this would then be trumped by the Golden Agouti's dominant 'A' , so all pups would therefore be 'Aa', which only left us with variables of 'P' and 'p' for the offspring to be either Argente Golden or Golden Agouti.

We can of course take this several steps further and use other gerbils with recessive genetics in which to test our Golden Agouti for various genes at the other loci. For example, with our Golden Agouti, if we wished to test for the presence of 'a' 'p' and also 'g' we would then use a Ruby-Eyed White gerbil, but our Ruby-Eyed White would definitely need to be 'aaggpp', as we know that there are several known genetic combinations that can dilute the coat to an off-white and the eyes to a ruby colour. So to do this seriously our Ruby-Eyed White would need to be bred as a pure strain and test crossed to other gerbil strains of known ancestry, all the time eliminating unwanted genes, and repeatedly back crossing to known strains to ensure that only the recessive genes that are wanted are carried in your 'aaCCDDEEppuw(d)uw(d)' separator gerbil.

A very well known colour strain in gerbils that was first developed by the Gerbil Genetics Group (G.G.G.), was the C-separator or as it later became known by fanciers as the Red-Eyed Silver Nutmeg, which was an odd and confusing description of the phenotype because it looked nothing like a Silver Nutmeg with red eyes, and is in reality a cream self coloured gerbil, and its genetics are 'aaCCDDeeppuw(d)uw(d)'. However the name has unfortunately stuck with it, but thank heavens breeders didn't decide to call their Pink-Eyed White colours by the fanciful names of Red-Eyed Burmese, or colourpoint Argente Goldens! In their course of research on gerbil coat colours, the G.G.G. developed several strains similar to this that enabled them to quickly identify the genes of any new colours of gerbils that appeared, as they effectively separate the genes of a gerbil of unknown ancestry.

The main separator gerbils used in the G.G.G's research were constructed after several years of intentional breeding for these valuable genetic "research tools" and includes the following genotypes and phenotypes as set out below:

aac(chm)c(chm)DDeePPuw(d)uw(d) - This gerbil looks like a washed out Silver Nutmeg, with more pigment on the extremities which you would expect from a colourpoint coat colour. Its eyes are dark and are similar to that of a Grey Agouti.

  • aaCCDDeeppuw(d)uw(d) - This gerbil is a cream self gerbil, and although you may have expected that ee would of brought another diluting factor into the fur colour, it does in fact add more yellow, which effectively gives it its cream colouring.
  • aac(chm)c(chm)DDEEppuw(d)uw(d) - This gerbil resembles the Ruby-Eyed White in coat colour.