The following points highlight the six main types of genes. The types are: 1. Complementary Genes 2. Duplicate Genes 3. Polymeric Genes 4. Modifying Genes 5. Lethal Genes 6. Moveable Genes.
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Type # 1. Complementary Genes:
Bateson and Punnett crossed two different white flowered varieties of sweet pea and obtained an F1 progeny of red flowered plants. On self-pollination the F1 plants gave an F2 progeny of 9 red and 7 white flowered plants. Single crosses between the red flowered variety and the two different white flowered varieties showed that the gene for red colour was dominant over the gene for each of the two white varieties.
The cross between the two white varieties can be explained by assuming two genes for red colour which must be present together, i.e., must act in a complementary way to each other. Thus each gene independently contributes something different but essential for synthesis of red pigment. If one of the two genes for red colour is absent, the result is a white flower. This explanation can be verified by making a checkerboard.
The inheritance of the colour of aleurone layer in corn also demonstrates interaction of complementary genes. The outermost layers of endosperm in the maturing corn kernels become modified into a specialised aleurone tissue, so named because the cells have rich deposits of aleurone grains. In corn the aleurone layer is coloured due to anthocyanin pigments in the cells, and is controlled by complementary effect of two genes.
Type # 2. Duplicate Genes:
When two or more genes have the same effect on a given trait, they are referred to as duplicate genes. In maize the gene for yellow endosperm is dominant over white endosperm. A pure breeding yellow endosperm plant when crossed to a white endosperm plant yields yellow endosperm in F1.
On self-pollination of F1 hybrids an F2 generation of 15 yellow and 1 white endosperm is obtained. The yellow endosperm results from two independent dominant genes Y1 and Y2. When any one of these two dominant genes or both together are present, yellow endosperm is produced.
When only recessive alleles are present in the homozygous condition (y1y1y2y2) it forms white endosperm. Thus the dominant genes Y1 and Y2 have an identical effect on endosperm colour and are consequently termed duplicate genes or iso-genes.
In human beings 3 different genes can produce up to 12 similar lactic dehydrogenase enzymes called isozymes or isoenzymes. Lactic dehydrogenase consists of four polypeptide chains each of which is coded for by two different genes A and B. A third gene C codes for yet another polypeptide chain that is present in lactic dehydrogenase found in male germ cells.
Type # 3. Polymeric Genes:
In Cucurbita pepo (summer squash) fruit shape could be spherical or cylindrical. The spherical fruit shape is dominant over cylindrical and is controlled by two independent genes. Thus there are two different varieties of spherical fruit plants.
When two such genetically different spherical fruit plants are crossed, the F1 progeny shows a novel fruit shape—discoid. Self-pollination of F1 discoid fruit plants produces an F2 generation with all the three fruit shapes, i.e., discoid, spherical and cylindrical in the proportion 9: 6: 1.
Out of the six spherical fruit plants of F2 generation, three plants belong to one variety and have the dominant gene S1. The other three spherical fruit plants belong to a genetically different variety with another dominant gene S2. Due to an additive effect of genes S1 and S2 (also designated as polymeric effect), the discoid shape is produced.
Type # 4. Modifying Genes:
As more and more instances of gene interaction were discovered, the earlier notion that one gene controls one phenotype independently of other genes had to be discarded. In reality an observed phenotype is the result of many complex processes within an organism. It is reasonable then that many genes should be involved in the final expression of a trait.
There is a large group of genes that come under a general heading or modifiers which influence the activity of other genes and change their phenotypic effects. The modifying effect may be quantitative so that the expression of a phenotype is either enhanced or suppressed.
There is a recessive suppressor gene (su) in Drosophila which suppresses the effect of a mutant gene for hairy wing (Hw) so that even homozygous flies (HwHw) fail to develop hair on their wings.
The same gene (it is also known as su-Hw) reduces the expression of a few other mutant phenotypes such as the ones caused by genes for interrupted wing veins and forked bristles. Another suppressor gene (su-S) in Drosophila is restricted in its action so that it reduces the expression of only one dominant gene which controls star eye shape.
In human beings the occurrence of minor brachydactylic (a form of brachydactylic in which only the index finger is of shorter length) in Norwegian families is due to a dominant gene B. There is a modifier gene M which modifies the effect of gene B to produce variable phenotypes.
Thus in individuals with both genes B and M, the index finger is very much shortened. Persons having gene B and recessive alleles of the modifier gene (mm) show only a slight shortening of the same finger. Modifier genes by themselves do not seem to produce a visible phenotype.
Type # 5. Lethal Genes:
Modifications in Mendelian ratios caused by interaction of genes. Lethal genes can also alter the basic 9:3:3:1 ratio and lead to death of an organism.
i. Dominant Lethals:
The yellow body colour in mice is dominant over brown, but the yellow mice are never true breeding. When yellow mice are inbred, the progeny consists of yellow and brown mice in the ratio 2: 1 which does not fit any of the Mendelian expectations.
Moreover, the litter size after inbreeding is smaller by one-fourth as compared to litter size resulting from a cross between yellow and brown. When yellow mice were backcrossed to true breeding brown mice, only heterozygous yellow mice were obtained.
Why were homozygous yellow mice never born? The answer came from a French geneticist L. Cuenot. He sacrificed Yy pregnant females after inbreeding and examined the embryos to determine if death occurred in embryonic stages or not. Indeed, one-fourth of the embryos were observed to die in late stages of development.
Thus only heterozygous yellow and brown mice in the ratio 2: 1 were being born. The ratio 1:2:1 expected when a cross between two heterozygotes is made was never obtained proving the lethal expression of the homozygous yellow gene.
The brachyury gene (I) in mouse is lethal in the homozygous state, and when heterozygous the animal survives, but with a short tail. Embryos homozygous for brachyury show complete absence of notochord, a few abnormalities and die in utero. When two short tail mice heterozygous for brachyury are crossed, the viable offspring produced show a phenotypic ratio of 2 short tail: 1 normal tail (Fig. 2.4).
In quite a few plants including maize, soybean and Antirrhinum (snapdragon) there is a dominant lethal gene which interferes with the process of photosynthesis and chlorophyll is not synthesised. Young seedlings which emerge from a seed carrying the homozygous dominant gene are yellow and die at a very young stage due to starvation. The heterozygous seedlings are light green in colour and able to survive. 
In all the cases of dominant lethal genes described above, the homozygous state of the gene leads to early death, whereas the heterozygote is viable. Perhaps the most serious effect a gene can have is to cause death even in the heterozygous state. The gene causing Huntington’s chorea in man expresses itself when a single dominant allele is present.
Whether homozygous or heterozygous, the phenotype of the disease becomes visible at middle age, usually after forty years. The individual suffers from muscular failure, mental retardation and finally death. Since the onset of Huntington’s chorea is much after the start of the reproductive period, the gene can be transmitted to the next generation of offspring.
Another dominant gene which causes epiloia in human beings leads to death in early stages of life even in the heterozygous condition due to severe mental defects, tumours and abnormal skin growths. Dominant lethal genes which express lethality at an early stage in life are not detectable in the population.
ii. Recessive Lethality:
The recessive lethal gene remains unnoticed in the population because it does not produce a visible phenotype in the heterozygous state. In fact it may be transmitted through heterozygous carriers for many generations without being detected. Consequently, a larger number of recessive lethal genes are known as compared to the dominant lethals.
There is a recessive lethal gene in man which causes death of newborn infants by producing internal adhesions of the lungs. A foetus homozygous for this gene completes its embryonic development with the help of oxygen supplied by the maternal blood. But death occurs soon after birth when the lungs fail to function normally.
Such a recessive lethal gene is carried in heterozygous individuals without producing harmful effects. It is detected only when two heterozygous persons marry and about one-fourth of their children die after birth, as they receive both recessive alleles from their parents.
Another recessive lethal gene in humans known as Tay Sachs disease causes death of young children. Individuals homozygous for this gene lack one of the enzymes needed for the normal metabolism of fatty substances.
The phenotype of the disease becomes visible after the first one year when fatty substances accumulate in the nerve sheaths. The transmission of nerve impulses becomes affected leading to loss of muscular control and mental deficiency. Within a few years the individual dies.
In humans there is a good chance of expression of recessive lethal genes in offspring of first cousin marriages. The single allele of the gene may have been present in the normal ancestors. It is only when the two alleles combine in the offspring of closely related persons that lethality is expressed.
In mouse hydrocephaly is due to a recessive lethal gene. During embryonal development there is abnormal growth of cartilage. This leads to irregularities in formation of skull and brain and excessive accumulation of cerebrospinal fluid. Embryos carrying the homozygous gene do not survive. The heterozygotes are phenotypically normal.
There is a recessive lethal gene in the beef producing cattle (dexter) in England. Dexter is the heterozygous breed which is highly prized for the larger quantity of beef meat it can produce.
The common breed of cattle known as Kerry has two homozygous dominant genes, is normal like the dexter but produces less meat. When two dexters are crossed the progeny consists of 1 kerry: 2 dexters: 1 bulldog. The bulldog calf carries two recessive lethal genes, has very short legs, a few abnormalities and dies soon after birth.
iii. Sex-Linked Lethals:
This is a system in which the lethal gene is carried on the sex chromosome, usually X. In Drosophila, sex-linked recessive lethals are frequently employed to detect mutations. A recessive lethal gene carried on the X chromosome is especially important in the hemizygous male individuals because it can express lethality when only a single allele is present.
The presence of a lethal X-linked gene can also alter the sex ratio so that more females are born instead of the expected ratio of 1 female: 1 male. Thus a female carrying a recessive lethal gene will produce a progeny in which one-half of the male offspring would not be viable.
The disturbance in sex ratio is clearly visible in organisms like Drosophila which produce a large progeny. In human beings, existence of sex-linked lethal genes is suspected in those families where female births occur far more frequently than male births.
In human beings lethal effects among the progeny may be caused accidentally by radiation (X-ray) treatment of the reproductive organs of the parents. According to a study by R. Turpin in France, when women receive X-ray exposures in the pelvic region for abdominal ailments, recessive lethal mutations are induced in the X chromosome present in the ovum. Such a woman produces more females and very few males in the progeny.
If the male parent is exposed to X-rays and dominant lethal mutations are induced on his X chromosome, there will be more boys in the progeny and few females. This is because the single X chromosome is passed to the daughters resulting in their death.
Muscular dystrophy (Duchene type) is due to an X-linked recessive gene which shows a visible phenotype many years after birth. Boys having this gene are normal for about 10 years after which there is failure of muscular control and death results.
iv. Conditional Lethals:
Sometimes an organism lives normally under one set of conditions, but when certain changes are introduced in its environment, lethality results. One of the first conditional lethals known was recognised by Dobzhansky in Drosophila pseudoobscura.
The flies live normally at a temperature of 16.5°C, but at 25.5°C the flies die. Similarly in the wasp Bracon hebetor the mutant gene which produces kidney-eyes at lower temperatures expresses lethality at a temperature of 30°C.
A number of conditional lethals have been described in Drosophila melanogaster by Suzuki in 1970. He has indicated that certain mutant strains became lethal when they were exposed to high temperatures only during the late larval stages. This is called the temperature-sensitive stage.
If the larvae are kept at low temperatures during the specific temperature- sensitive stage, the flies born can live normally even at high temperatures throughout their life cycle.
Perhaps a specific gene product—an enzyme or a protein becomes altered, causing death if the larvae are exposed to high temperature during the critical period. In fact with this perspective, conditional lethals are being studied extensively in micro-organisms for analysing genes, enzymes and proteins.
In poultry there is a recessive gene which causes feathers to break off. Chickens homozygous for this gene become devoid of feathers but are able to live normally if they are kept in a relatively warm environment. But if the temperature falls below the optimum, the chickens die due to lack of insulation provided by normal feathers.
Conditional lethals have been well studied in some haploid organisms such as yeasts, Neurospora and others. It is easy to study lethal genes in haploid organisms because the presence of even a single allele results in lethality.
The wild type Neurospora is able to grow on a medium deficient in the amino acid arginine because it produces all the necessary enzymes required for synthesis of arginine from sugar and ammonia.
But a mutant strain of Neurospora will not be able to grow on the same medium. A strain of yeast that grows normally on a glucose medium can show lethal effects if grown on a medium containing galactose. The mutant gene therefore, acts as a conditional lethal.
v. Early and Late Acting Lethals:
The earliest stage at which lethal genes can act is evident from studies on mutations in gametes. Normal gametes are more viable and have better chances of effecting fertilisation and producing zygotes. The lethal genes are eventually lost with the death of un-fertilised gametes. Such genes are referred to as gametic lethals.
The phenomenon by which a certain class of gametes is specifically inhibited from taking part in fertilisation has been termed meiotic drive by Sandler and Novitski. There is a gene called segregation distorter (SD) present on the second chromosome of Drosophila. The dominant allele of this gene does not allow gametes to participate in fertilisation.
Thus only gametes bearing the recessive allele (sd) are able to fertilize eggs and produce viable zygotes. Since this also results in distortion of typical Mendelian ratios, the name segregation distorter has been given to this gene.
There are lethal genes that act after zygote formation resulting in embryonic death. In experimental animals such as the mouse, it is possible to determine this lethal effect by sacrificing impregnated females and analysing the dead embryos.
If, however, death occurs very early in embryonal development, this technique does not succeed because actual observation of aborted embryos is not possible. There is a gene which exerts a killing effect by preventing normal cleavage of the zygote. Such a gene is called a zygotic lethal.
In human beings the gene described for causing adhesions in lungs expresses lethality soon after birth when the lungs of the newborn infant fail to function normally. In plants most lethal genes are known to act during or after seed germination.
Among late acting lethal genes, some clear cut examples can be cited from human diseases. Genes causing muscular dystrophy (Duchene type) and Tay Sachs disease cause death before or in the second decade of life, before the onset of reproduction. Huntington’s chorea on the other hand is fatal when the person is middle-aged, and the gene may have already been passed on to future generations.
Type # 6. Moveable Genes:
There are genes or segments of DNA that can become incorporated and function at a number of locations on the genome. The F factor can integrate at specific sites on the E. coli genome. Molecular studies have shown that the F element consists of three different functional blocks of genes.
One region contains genes necessary for transfer of F element through conjugation from one bacterium to another. A second region controls autonomous replication of F. The third region contains a number of different insertion sequences (IS). The integration of the F factor is brought about by a recombination between one of the IS sequences on the F factor and an IS sequence on the host chromosome.
The IS sequences are themselves moveable DNA segments which can be inserted at a large number of sites in different chromosomes. There are a number of IS sequences known of which 3, IS1, IS2 and IS3 have been studied in considerable detail. These range in size from 700 to 1400 base pairs.
When an IS sequence is inserted into a gene, it breaks the continuity of the gene sequence, and may or may not inhibit expression of the gene. IS sequences also exert some effect on adjacent genes.
More often the adjacent genes are inactivated; sometimes however, a previously silent gene could become activated. IS sequences appear also to be hot spots (vulnerable locations) for deletions; they are also involved in a number of recombination phenomena.
Another group of moveable DNA segments, many of which carry drug resistance genes are called transposons. They were probably first discovered in plants as controlling elements in maize, but were clearly demonstrated first in bacteria. In 1974 Hedges and Jacob found that when a gene for resistance to antibiotics like penicillin and ampicillin was transferred from one plasmid to another, it resulted in an increase in the size of the recipient plasmid.
The length of a typical transposon is several kilo bases, a few are much longer. Much of the widespread antibiotic resistance among bacteria is due to the spread of transposons that contain one or more antibiotic resistance genes. When a transposon mobilises and inserts into a conjugative plasmid, it can be widely disseminated among different bacterial hosts by means of conjugation.
Some transposons have composite structures with antibiotic resistance sandwiched between insertion sequences. Transposons are usually designated by the abbreviation Tn followed by an italicised number, for example Tn5. When it is necessary to include the name of the gene it carries in its designation, it becomes Tn5 (neo-r, str-r) to reflect presence of genes for resistance to neomycin and streptomycin.