May 16, 2009

An Introduction to Practical Animal Breeding: Part II. Basic biology

Agriculture, New Zealand, farming, animal breeding, genetics, livestock improvement, theory, practical advice, basic biology, Mendel, Mendelism, chromosomes, genes, terminology.

By Dr Clive Dalton

PART II Basic biology


Basic biology
The cell is the basic component of all living tissue. Its discovery, which led to the 'cell theory', occurred in the 1830s and was followed by great advances in biology and genetics. Inside the cell wall is the jelly-like protoplasm and in the centre of this is the cell nucleus, the control mechanism of life itself. Fig. 6 shows the main parts of the animal cell.

Within the cell nucleus is the chromatin from which the thread-like chromosomes develop. On these chromosomes are the genes which are the units of inheritance. Genes can be visualised as beads on a string, the string being the chromosome. Fig. 7 is a drawing of what genes or groups of genes look like on the chromosome under a powerful microscope.

In 1953 the chemical structure of a gene was proposed. This is the now well-documented substance called DNA (deoxyribonucleic acid). Biochemical genetics has made great strides in recent years and has progressed into genetic engineering, in which genetic material can be exchanged from one organism to another or perhaps even synthesized in future. There is both excitement and concern over future prospects in this area.

Cells are broadly classified into body cells and germ cells. Body cells are concerned in the main structure of the animal whereas the germ cells are the spermatozoa (sperm) of the male and the ova (eggs) of the female.

Each animal species has a definite number of chromosomes and these are arranged in pairs (called homologous pairs) in the cell nucleus. For example, man has 46 chromosomes (23 pairs); the dog78 (39 pairs); the pig 38 (19 pairs); cattle 60 (30pairs); the horse 64 (32 pairs); the donkey 64 (32 pairs); the sheep 54 (27 pairs); the goat 60 (30 pairs).

The formation of these chromosomes in the cell nucleus is now a well documented routine. It is possible to have chromosomes examined (called karotyping) for defects of shape or missing parts. This is especially valuable in human genetic counseling, for example to predict the chances of parents producing mongo1 children.

When body cells divide in the normal process of animal growth, the chromosomes are halved by splitting down their length into chromatids, and equal numbers of these halved chromosomes are drawn to either end of the cell which then constricts between the two new nuclei. This produces two new cells, each with the same number of chromosomes as the parent cells, and the process is called mitosis.

In the formation of germ cells or gametes, the process is different from mitosis as the germ cells end up with only half the number of chromosomes that are present in the body cells. This reduction happens during a second division (see fig. 8). This ensures that when a new offspring is formed from the united sperm and egg, it finishes with the correct number of chromosomes for the species. This is called meiosis, or 'reduction division'. Fig. 8 contrasts the two processes.

Correction: The large letter P below Mitosis is an error created in scanning. It should read 2n as under Meiosis,

When the female cells divide in meiosis, one half produces the ovum and the other half is thrown out of the cell as a polar body. In the division of male cells, nothing is wasted and each half produces a sperm. The challenge comes later for the sperm for although there are millions available to fertilise an ovum, only one actually carries out fertilization while the remainder die (fig. 9).

The term diploid is applied to the double chromosome (or normal) state (e.g. 54 chromosomes in sheep), while haploid is used for the germ cells that carry half this number of chromosomes (27in sheep). A gamete is the male or female germ cell. When these gametes combine, the result is called a zygote.

There are two broad classes of chromosomes - autosomes or ordinary chromosomes, and sex chromosomes that specifically control the sex of the offspring. In all species except birds, butterflies and some reptiles, the male determines the sex of the offspring. Thus, in farm animals the sire is the sex determiner. The exception is poultry where this is reversed and the female is the sex determiner. The letters X and Y are used to describe the sex chromosomes. The dam carries only the X chromosomes (described as XX), and the sire carries both X and Y in equal proportions (described as XY).

These chromosomes can be recognised by examination with a microscope. Fig. 10 is a drawing from a photograph of the chromosomes of a domestic ram. The photograph has been cut up and the individual chromosomes laid out from largest to smallest. Note the 26 pairs of chromosomes, then the single X and the single Y (much smaller than the X). There are accordingly 26 pairs plus (X +Y), making 27pairs, or 54 in total.

Thus when a sire mates with a dam, the result is this:

Note here that the sire is producing X and Y gametes in equal proportions.

The result is males and females in equal proportions but the scientific theory stresses that this is what happens 'on average' and when there are plenty of offspring to test the result. Generally if there is a run of males, this will be counterbalanced by a run of females later.

However, there are exceptions to this rule when occasionally sires produce an abnormally high or low number of sons and this may be due to some defective mechanism in the Y-bearing gamete. In general, though, imbalanced sex ratios (i.e. not 50 : 50) are the result of insufficient observations.

To work out this ratio, and for the discussion of Mendelism later, it may be advisable to practice how to draw the lines in these crosses to get the right answer and note where the answer is written.

Thus in the example given previously:

(I) is crossed with (3) and the answer written under (1)
(1) is crossed with (4) and the answer written under (2)
(2) is crossed with (3) and the answer written under (3)
(2) is crossed with (4) and the answer written under (4).

Another way of obtaining the answer is to lay it out in a square or checker board where the results of the crosses are put in each box.

Normally, the ordinary chromosomes (the autosomes) occur in homologous pairs. However, it is possible to have a situation where more than two chromosomes are present and this is called polyploidy. There are a number of different kinds of polyploids, depending on the number of chromosomes present. For example, for three chromosomes denoted by a, b and c, there could be:

Monoploid: a b c
Diploid: aa bb cc
Triploid: aaa bbb ccc
Tetraploid: aaaa bbbb cccc and so on.

The process of multiplying the number of chromosomes can bedone by chemical treatment of the cells and has been exploited in plant breeding where highly productive polyploids are marketed commercially. Viable polyploids are not currently found in farm animals.

Changes can occur within any one chromosome such as deficiency (where a part is lost), duplication (where a part is added), translocation (where parts of two different chromosomes exchange) and inversion (where parts of the chromosome change). All these changes lead to complications at cell division. (For full information see Sinnot et al.(Ref 6) and Strickberger.(Ref 7).

Mendel's genetics: Mendelism
The detailed discoveries of Gregor Mendel in his experiments with garden peas in the 1860's have been well documented (Ref 6 and 7). The main feature for animal breeders to remember is that Mendel's discoveries (termed Mendelism) were based on simple, clearly-defined traits that were inherited as separate entities. These were traits such as colour (either red or white), stem length (short or tall) and skin shape (round or wrinkled) that were controlled by single genes.

It is interesting to note that Mendel did record that there were some 'characters that did not stand out clearly'. Perhaps it was fortunate that he avoided working on these and concentrated on single-gene traits. With only a monastery garden as his laboratory Mendel's achievements were prodigious indeed.

One of the major aspects of Mendel's discoveries was to show that the 'choosing' of genes from each parent was controlled entirely by the laws of chance. This profound discovery has been the foundation of all subsequent work and although we know of the exceptions such as linkage, it is still sobering to think of the importance of chance.

There is an extensive vocabulary of technical terms that is now part of Mendelism. These terms are fully explained and discussed in relation to current genetics in other texts (Ref 6 and 7). A few of the terms are discussed here as they are needed to understand the basic concepts of animal breeding.

The two or more alternative forms of agene are called alleles. The word allele means alternative. The position on the chromosome where they are found is called a locus (plura1 is loci). Unfortunately gene and allele are sometimes used as interchangeable terms although to do this is not strictly correct.

A correct description of the gene for coat colour in cattle for example would be to say that it is present as either the dominant allele black (B), or the recessive allele red (b). Another example is the three haemoglobin blood types in sheep described as A, B and N. This is called an allelic series as there can be the following pairs of alleles HbA, Hba, HbB , Hbb, HbN , Hbn. In cattle blood groups at the B locus more than 250 alleles have been described.

A homozygote is an individual that has identical alleles at a specified locus e.g. AA or aa. A heterozygote is an individual that has non-identical alleles at a specified locus e.g. Aa.

A dominant allele covers over or masks the effects of a recessive allele. However, recessive alleles do not always stay covered as they can appear in later generations. There are many examples of dominant and recessive alleles in farm animals. A few very general examples are show in table below.

CATTLE: Dominant allele versus Recessive allele
Polled (absence of horns) v Horns (presence)
Black coat v red coat
White head (Hereford) v plain head
Black and white Friesian v red and white Friesian
Normal size v drawf
Normal palate v cleft palate
Normal pastern v bent pasterns

White fleece v black fleece
Self colour v black spotted
Hairy (medullated fleece) v non medullated
Normal leg length v short legged Ancon
Polled v horned
Normal cover v naked

Grey coat v bay coat
Bay coat v black coat
Black coat v chestnut coat

White skin v black skin
Lop ears v prick ears
Normal nippes v inverted nipples

The naming of genes
The main system of coding genes is to use letters. Usually capital letters are given to dominant alleles and small letters to recessive alleles.

P = polled allele: p = horned allele
W =white allele: w = black allele

In the animal to show the diploid or double stateof the alleles, two letters are used.

PP = polled cow: pp = horned cow
WW = white sheep: ww =black sheep

Some text books on genetics use mathematical symbols separated by strokes. A plus sign (+) is used instead of the normal allele (sometimes called the wild type) so that if P is regarded as normal, then +/+ is the same as PP. The small letter may still be used for the recessive allele so that +/p is the same as Pp.

In recent years a convention has developed whereby capital letters are used for the gene locus and a small superscript is used to distinguish the allele. Many genes have been named after the person who discovered them or where they were discovered.

Examples of the latter are the blood groups discovered in the Lutheran community Lua and Lub, or the hairy (medullated) gene of the New Zealand Drysdale sheep (N) found on Mr Neilson's farm. This gene N is suggested as an allelic series coded Nj, Nt, Nd and n (the non-hairy). In some cases to avoid confusion, the proposed names for genes have to be submitted to an international indexing body for approval so that the identity of each gene is unique.

Mendel's mathematics and more terminology
To explain the ratios obtained from traits controlled by single genes, the polled and horned alleles are again used. The capital letter P is used for the polled allele. Polledness is the absence of horns and is found in cattle, sheep and goats.

The polled allele (P) is generally dominant to the allele for presence of horns denoted by the small letter p. Note that ‘p’ denotes presence of horns -it does not control the size and shape of the horns or scurs that may grow. These are controlled by many other genes. However, for simplicity in this discussion ‘p’ is used to denote horns.

P = polled (absence of horns)
p = horned (presence of horns)

PP = homozygous (both alleles identical); dominant (both capital letters present); so it is a polled parent.
pp = homozygous (both alleles identical); recessive (both small letters present); so it is a horned parent.

In the cross the results are:

Pp = heterozygous (alleles non-identical).
Dominant P prevents expression of recessive p so the offspring all looked polled - but they are heterozygous.

Mendelism uses the term phenotype to describe what an animal looks like -its physical form, its colour or its behaviour. The term genotype is used to describe the genetic factors that influence its phenotype. In farming terms, the phenotype is what you can see in the animal; the genotype is what is carried in the cells (testicles and ovaries) of the animal.

In the previous example, for the

PP animal - phenotype and genotype are the same
pp animal - phenotype and genotype are the same
Pp animal -phenotype looks polled but genotype is not pure polled.

All the texts on genetics mentioned in the bibliography cover in full what happens when genes segregate and combine with other genes but the main points are covered here.

Using the single pair of alleles (polled and horned) on separate chromosomes, the results of segregation are as follows:

polled x polled (PP x PP) PP All polled - homozygous
horned x horned (pp x pp) PP All horned - homozygous
polled x horned (PP x pp) PP All polled - heterozygous

In the crosses between homozygotes (PP x PP) and (pp x pp), the offspring are respectively all PP and all pp. This is often described as 'breeding true to type'. On the other hand, in the mating (PP x pp), the parents do not breed true to type.

However, care is needed in using this term 'true to type' for although it may be clear in the Mendelian sense, it is also used by breeders to describe pre-potency or the ability of an animal(usually a sire) to produce offspring like itself and can be much more complex. Crossing the two heterozygous polled animals (Pp) gives this result:

The ratio between the genotypes is (l : 2: 1) as shown, but the ratio between the phenotypes is (3 : 1) because the breeder cannot tell the Pp from PP as they are both polled. Thus the Pp parents have not 'bred true'; they have bred other types of animals as well as those like themselves.

With two pairs of alleles on separate chromosomes the situation becomes a little more complicated.

An example would be the crossing of Angus and Hereford cattle. The Angus carries the black coat and polled alleles, that are dominant over the Hereford's allele for red body colour and horns. Note that the white head colour of the Hereford is a separate dominant allele. The results of a cross are:

When these heterozygous animals are crossed, the results are these
9 Black polled (cells containing B and P)
3 Red polled (cells containing bb and P)
3 Black horned (containing B and pp)
1 Red horned (cell containing bb and pp)
This is Mendel's (9 : 3 : 3 : 1) ratio. The combinations down the diagonal of the box are important; those at either end marked (1) are identical to the original parents, and the two in the middle marked (2) are new combinations -in this case red polled and black horned.

Note that white heads would appear in some of these animals but not in all of them. This would be independent of coat colour and the horned/polled status. The parent generation of a series of crosses is described as P and the next generation as FI or the ‘first filial’ or daughter generation. When the F1 generation is bred from, this gives the F2 or "second filial generation" and so on to F3, etc.

Mendel's laws of segregation go further. By using the box layout it can be seen that with four genes the ratios are (27 : 9 : 9 : 9 : 3 : 3 : 3 : 1).

The situation now is best described by a general formula that says where n = the number of genes, there are 2n gametes and 3n genotypes. The value of n is how many times the value 2 or 3 has to be multiplied by itself to give the answer. This is shown as follows:

The action of lethal genes causes either the death or physical injury of the animal. Genes that cause injury or maiming may be called semi-lethal as the animal does not always die. Death from lethal genes may occur before birth (in utero or in the shell), in very early life or in later life. Modern surgical skills may now keep animals alive that would formerly have died so the division between lethal and semi-lethal genes may not be definite any more. There are many examples of these lethal genes (Ref 8).

• Dropsical (bulldog) calves in cattle
• Imperforate anus in pigs and sheep
• Hydrocephalus in cattle, sheep and pigs
• Cleft palate (general)
• Nakedness in poultry
• Hairlessness, amputated limbs (general)

Lethal genes that act before birth may be difficult to determine but their presence is usually suspected by the fact that certain predictable genotypes are not seen in the offspring. Care is needed though to ensure that sufficient offspring have been examined before any pronouncements are made, otherwise one could misinterpret chance effects as being the actual cause of the problem. The lethal action of genes can have a 'dominant effect' where it is seen in the phenotype, but the action can also have a 'recessive effect' where the results are not obvious in the phenotype. This latter case is the more difficult to determine. For example:

For a dominant lethal allele D:
  • DD dies
  • Dd dies
  • dd lives
Here those having the dominant allele (capital D) die.

For the recessive lethal allele 1:
  • LL lives
  • Ll lives
  • ll dies.
Here, those having the dominant allele (capital L) live and those carrying the recessive allele (small 1) die. The L1, the heterozygote, lives because of the dominant allele L, but is a 'carrier' of the recessive lethal allele 1.

Some genes that lie on the same chromosome appear to be transmitted as a group. This phenomenon is called linkage and the genes are said to be 'linked'. This means that the independent assortment of genes featured by Mendel does not always apply, and an offspring may not get a completely random sample of its parent's genes.

The main points about linkage are that while making it harder to get some new combinations of genes it also makes it easier to hold on to existing ones. Lush (Ref 9) likened linkage to friction -it can slow up an engine but is very useful in brakes.

Crossing over is the phenomenon of transferring these linked genes from one chromosome of the pair to the other duringcell division and is fully described in all texts on genetics (e.g. Strickberger7). A simplified explanation of crossing over is as follows.

Consider two parental chromosomes with genes arranged along them. The action happens in the three stages illustrated in fig. 11.

The sections of the chromosomes that cross over are called chromatids. Crossing over is a breaking-up process among genes that are linked, and tends to bring each pair of alleles into random distribution with every other pair (Ref 9). Thus crossing over has a long-term mixing effect on all the genes.

Besides determining the sex of the offspring, the X and Y chromosomes can carry genes that affect other traits. This means that the expression of certain characters is affected by the sex of the offspring. This is called sex linkage but should not be confused with traits that are sex limited. good example of a sex-limited character is milk production which males cannot express because of restrictions in their physiology.

Where a gene is carried on the larger X chromosome there may be no corresponding gene on the smaller Y chromosome. This is often drawn by using a bar on the X like this:

Here the male will show the effect of the single allele of the gene, regardless of whether it is dominant or recessive. It is as if the Y chromosome in the male had no power. In the female, what is actually expressed in the phenotype is what is expected from the genotype.

When a gene is carried on the Y chromosome, only the male will show the effect of the gene and-it will be passed on from the father to the son. It is very important to know whether the sex-linked gene is dominant or recessive as the situation is different in its transmission.

The main practical point is that if the allele is dominant, every affected offspring has an affected parent i.e. it is seen in every generation. If the allele is recessive, the gene appears to 'skip generations'. Two classical examples are severe rickets (a dominant sex-linked gene) and red-green colour blindness (a recessive sex-linked gene) in humans. (Ref 10 and 11).

Sex linkage had been widely used in poultry in the past as an aid to separating the sexes of day-old chicks. Here the sexes could be separated by feather colour rather than by examination of the chick's vent. The colour genes most commonly used in this were the dominant 'silver' allele and the recessive 'gold' allele. Genes for 'barred' colour were also used. These appeared on the wings and back. The term 'auto-sexing' was sometimes used to describe all these genes (Ref 12).

It is possible to map the genes on a chromosome using the fact that the closer together two genes are on a chromosome, the less chance there is of an exchange formed between them, and the less chance of recombination occurring. So if heterozygotes are mated and provided there are plenty of offspring (this is no problem in laboratory fruit flies), then the percentage of recombinants is an approximate measure of the distance the genes are apart.

By considering a series of crosses involving known linked genes, it is possible to map the chromosomes showing the serial order and approximate distance apart of the genes. Chromosome mapping is usually done with three linked genes. Texts on genetics should be referred to for full details (Ref 7).' Although chromosome mapping is well advanced in fruit flies and in maize, it has not yet been exploited in animals but could be useful for the future.

A mutation is a change in a gene. Mutations give rise to new alleles at particular loci. Thus mutations are the principal means of producing new heritable variation. There are four main groups of mutations, based on where they happen. These are:

(a) Within the gene i.e. 'intragenic' or 'point' mutations.
(b) Changes in groups of genes on a chromosome.
(c) Changes in the whole chromosome.
(d) Changes in a whole chromosome set.

Studies have shown that genes mutate spontaneously at rates which are generally constant for a particular gene but vary from gene to gene. Mutations can be reversible, but the rates of mutation in the two directions are usually very different. A mutation rate for a gene is generally low, for example, from 1 in 100000 to 1 in a million.

Albinism in man (a recessive gene) is estimated as occurring 28 mutations per million gametes per generation, whereas deaf-mutism which involves many loci is predicted as 450 per million (Ref 11).

There is a number of factors that are known to cause mutations such as certain ionising radiations, abnormally high or low temperatures, certain chemicals, other genes carried by the organism or ultra-violet light (non-ionising radiation). Up to the present these effects have only been studied on bacteria, fruit flies and plants, but interest in their effects on animals will increase in future. Increasing radiation and chemicals would be the most likely methods used to cause mutations in animals either through accidental spillages or designed experiments.

There are many examples of mutations in animals. All the examples given earlier as lethal or semi-lethal genes arose from mutations. Some mutants have been made into new breeds or types. The short-legged Ancon sheep is a classical example as are dwarf cattle and horses. Among the wide range in dog breeds are some examples of mutants that have been established as new breeds.

How many genes concern breeders?
Mendel confined himself to single-gene traits and developed his theories for situations involving a limited number of combinations of genes. With farm animals, breeders are generally dealing with thousands of genes and an almost infinite number of possible gene combinations depending on the traits considered.

In the fruit fly it is estimated that there are about 6000 pairs of genes on its four chromosomes. Hence in a cow with 60 chromosomes the number of genes must be enormous. Farm animal breeders accept that they are concerned with many genes and this leads into the area of population genetics to be discussed in Part 111.

The way in which genes work is not clear and there are many things still to explain, for example how cells that have similar chromosomes end up as parts of vastly different organs all having different functions.

Biochemical geneticists have shown that the main form of gene control is through enzymes. These are the proteins which seem to act as triggers or accelerants to get the function and the animal moving. It also seems that certain genes do not act all the time - they need to be 'switched on' and 'switched’ off.

Examples would include genes that change coat colours in arctic animals with the approach of winter. There is evidence that certain genes can act to block certain actions of enzymes and these are called 'genetic blocks'. One example is the dominant allele of a gene that allows some people to taste a group of chemical compounds while some others are 'non-tasters'. Tasting the chemicals is useful clearly as a test for the presence of the gene. The genes involved seem to produce different biochemical side-effects or blocks. Clearly, there must be similar situations in farm animals that have yet to be identified.

Pleiotropy is a special situation which is found where the same gene has different effects on different traits at the same time. A very good example of known pleiotropy is in the New Zealand Drysdale sheep which has a very strongly medullated (hairy) fleece which is ideal for carpets. However, it has the disadvantage of having very strong horns in the males and smaller horns in the female which cause problems at shearing and in skinning after slaughter. Both the hair and the hornsare due to the same N gene so in this pleiotropy there is little chance of selecting for hair while eliminating the horns.

The genetic situation in British hairy and horned sheep breeds has not been so fully investigated as in the Drysdale so it may not be a case of pleiotropy. Indeed, much more is known about pleiotropy in the fruit fly and blood group antigens than about economic characters in farm livestock. A point worthy of note is the contrast between linkage(where gene combinations can break up) and pleiotropy where they do not.

Gene interaction is said to occur when the same trait is affected by more than one pair of genes (alleles), and these genes may affect each other (interact) in the development of a trait.

These different genes are found at many different loci on different chromosomes; and although they may be independent in their segregation, they may not be independent in their action; i.e. they appear to act together to produce the trait. The complexity of the economic traits in farm animals is such that gene interaction must be a major feature although completely documented cases to use as examples are difficult to find.

Genetics textbooks usually discuss a number of different kinds of dominance along with a description of pleiotropy and gene interaction (Ref 13).

Complete dominance is the first kind and is that already described when the homozygous and heterozygous dominants AA and Aa equally mask the recessive allele aa.

Overdominance is where the heterozygote Aaperforms better than either homozygote AA or aa. This situation is a possible explanation of why some crossbreds or hybrids show superiority in fitness traits.

The other kind of dominance is incomplete dominance or no dominance. These are considered by some authorities to be similar, but others consider them to be different. A good example of this is coat colour in Shorthorn cattle. The coats of Shorthorn cattle are either red, roan (a mixture of red and white hair) or white. The situation is like this:

Dominant red = RR
Recessive white = rr
Heterozygous roan = Rr

RR x RR = all red (RR)
Rr x rr = all white (rr)
Rr x Rr = 1RR (red) : 2Rr (roan): 1rr (white)

Here the phenotypic ratio 1 : 2 : 1 is the same as the genetic ratio – the heterozygote roan can be distinguished from the red. Certain breeds have been founded on these heterozygotes, for example - Blue Albion cattle where blue (Bb) is the heterozygote of black (BB) and white (bb). The blue Andalusian fowl is another example.

Epistasis acts rather like dominance where one gene masks the expression of the other (both on the same chromosome). Whereas dominance relates to alleles at the same locus, epistasis concerns genes that are not alleles. The masking gene is described as epistatic to the masked gene. Such genes that do not work in allelic series are very interesting because they modify the size and the direction of each other's effects. Some act as inhibitors and others are described as having 'threshold effects' where they can hold down the expression of other genes.

There are many examples of epistasis, the classical example being feather colour in poultry, when two breeds which were once very common in commercial practice are crossed. These are the White Leghorn (WLH) and the White Wyandotte (WW). Both are white but the WLH is genetically a coloured bird with a gene that masks the expression of colour, termed 1 (a colour inhibitor). This gene is epistatic to C (a colour producer). The WW is a true albino with no colour genes.

The results from the crossing are these:

9 offspring with I and C (white)
3 offspring with ii and C (coloured)
3 offspring with I and cc (white)
1 offspring with ii and cc (albino)

The ratio is 13 white (including the albino): 3 coloured. Thus epistasis is seen as a phenomenon that alters the classical 9:3:3: 1 ratio.

Heredity and the environment
The subject of heredity (genetics) and the environment is amajor theme that underlines all work in animal breeding and is discussed in Part 111. The main point to make here is that most traits expressed in livestock are due to the influence of both heredity and environment working together. The fact that they work together must be stressed.

Genes cannot be affected directly by the environment. For some years, it was believed by the Lysenko school of Soviet geneticists that the environment could directly affect genes. The basis of this belief was that if a crop was grown on good land, then the seed from it would have absorbed a 'superiority' (presumed to be genetic) that it would then always have, and it would pass this on to the next generation.

Similarly docking lamb’s tails would eventually produce sheep that did not grow tails. Clearly this is not acceptable and is now under universally accepted that the environment cannot affect genes directly. Genes can only provide the message and direction for the development of the animal’s phenotype. The actual expression of the gene is controlled by the environment, for example temperature, light, feeding and management.

However, it may be wise to keep an open mind for the future because among the complexities of the environment something may yet be discovered that can directly affect the animal’s genotype. This subject is considered by Lerner (Ref 14).

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