Bid Napper

ebay bidding

Line breeding and its place in Breed Development

Excerpts from ‘Genetics for Cat Breeders'; by Roy Robinson M.I. Bio

Chapter VII - ‘Elimination of Anomalies’

Everyone is agreed that it is desirable to eliminate genetic anomalies. Yet, they appear to persist tenaciously. Why should this be so? The reason is two-fold: firstly, the problem can be more complex than appears on the surface and, secondly, the remedy may demand more drastic action than is acceptable. Somewhat different problems arise and different procedures should be followed according to the known or assumed ode if inheritance. That is, whether the anomaly displays (1) dominant, (2) recessive monogenetic heredity or (3) polygenic heredity.

With dominant monogenic heredity, there is no problem when the disorder is readily apparent or is regularly manifested. However, this is not always the situation. For example, the affliction may not be evident until late in life. Until after puberty ad the animal has been breeding for some time. This latter aspect can only be tackled by means of clinical analysis designed for early diagnosis of onset of the disease. Also, of course, the conscientious seeking and taking notice of such clinical reports. It is silly to ignore a positive report simply because and outstanding cat is apparently healthy. Eventually, it will not be and, meantime, the genetic damage it can do is considerable. The case of irregular manifestation is similar except that clinical diagnosis is excluded. Bodily, the animal is fit healthy and detection is probably best handled by the same methods as recommended for that of finding carriers of a recessive anomaly.

Theoretically, all dominant monogenic anomalies could be eliminated if all of the descendants of subsequently afflicted animals are prevented from breeding. This would be drastic action indeed when it is considered that about fifty pre cent of the animal’s descendants will be free of the anomaly. Unfortunately, the price to be paid is that the other fifty percent will be handing on the anomaly until they are eventually detected. Fortunately, it is possible that the cat is not troubled with this sort of anomaly. It is to be hoped that this will always be so but, alas, this cannot be taken for granted. For instance, progressive retinal atrophy is a late developing genetic disease of the eye in doges. In a few breeds, the disease is troublesome and the main factor for this is that the young fog can see perfectly but eventually becomes partially or totally blind. The late onset of the affliction means that the animal may have bred before the first symptoms are noticed. A similar disease could occur in the cat.

With recessive monogenic heredity, the problem is that of detection of the heterozygote or “carrier”. It is not a question of clinical detection since these animals are fully normal. Their detection lies in another direction: that of test mating. This may be accomplished in one of two ways. If the anomaly is slight (undesirable, say but not crippling) and does not interfere with reproduction, the animal to be tested can be mated to one or more affected animals. Provided sufficient normal kittens are produced, without the appearance of a single anomalous individual, the animal may be judged not to be a carrier. The number of kittens to be bred in each test will depend upon the level of acceptable error. It may be that a carrier animal could produce entirely normal young by chance. However, the chances of such an event become smaller as the number of kittens increases. This is the error which must be made acceptably low by stipulating that a certain number of young be bred. Column A of the accompanying table gives the error for successive normal kittens examined. Two acceptable levels are 5 per cent (5 kittens or more) and 1 per cent (7 kittens). The latter is preferable to the former as the and there is a strong case for making it mandatory.

When the anomaly is severe, breeding from such individuals may be either unethical or impracticable. A different procedure should be followed. This consists of mating the animal to be tested with known carriers. Again, the matter of acceptable error must be decided. Since this procedure is more roundabout, the number of kittens required must be increased, Column B of the table shows the error for successive normal kittens examined. The two levels of 5 per cent and 1 per cent require that t the rearing of 211 ad 17 kittens, respectively. It should be apparent that the kittens produced by these test matings should not ordinarily be used or sold for breeding since all of them will be carriers in the first method if testing and 50 per cent at least in the second.

Now, for various reasons, it many not be convenient to keep known carriers, yet it may be felt desirable to test certain animals, this can still be done by a method which is practicable for males. The procedure is to mate the male to a number of his daughters (which need not necessarily be from the same mother). The error involved here is a two stage affair, (1) that of not mating the male to a carrier daughter (only half of the daughters will be expected to receive the suspected recessive gene) and (2) that of not breeding at least one anomalous kitten. To calculate the error, it is necessary firstly to find the value for each daughter according to the number of kittens she has produced. This is shown by column C of the table. The error for the male is derived by multiplying each of these values together. Thus, suppose it has been possible to mate a male with four daughters and the various litters result in totals of 3, 5, 6 and 7 young per daughter, the values of C from the table are 71, 62, 59 and 57 respectively. The error for the male, therefore I, is the product of these, namely, 15 per cent. For totals of this average size, it would require 7 daughters to reduce the error to below the 5 per cent level.

This last test is often the one carried out in practice, In terms of numbers of kittens required to attain a certain minimum error, the test does not compare in efficiency with the two described earlier. However, it has an advantage not possessed by these, namely, that the test would reveal any recessive anomaly carried by the male, not just one in particular. This fact gives the test an added appeal. It may be objected that the test could not be performed by a small breeder, or possibly not repeatedly by medium or large breeders. I this case, it might be advisable for several breeders to band together and form a breeders’ cooperative as far as testing-mating of outstanding males is concerned. If this is not practicable, a breed society could take matter in hand and arrange a scheme of test mating. Certified males should commend (and deserve) increased stud fees. Adequate means if independent assessment would have to be devised to avoid deceit and to assure the correct operation of the scheme.

In practice, it is rarely possible to test mate females. This is unimportant if a male can be properly tested and pronounced free of genetic anomaly. No matter how many carrier queens he may mate, none of the offspring will be anomalous. Some of the carrier queens will produce carrier offspring but this cannot be avoided. It means, however, that the stud males must be test mated in each generation before being passed into general service. This testing will have to be continued until such time as the breed is judged to be free of the anomaly. It is difficult to be certain hoe many generations will be required. In part, it will depend upon the prevalence of the anomaly before the test mating was instigated. The values in the table are for recessive genes whose occurrence are up to expectation. Not all anomalies behave in this manner. Some so weaken the individual that they die before (for example, in utero) they cannot be recorded. Also, certain individuals may have the gene for an anomaly yet fail to show it. In these circumstances, the values of the table are too optimistic. They are methods of tackling this complication but they are beyond the scope of this book. Whenever such a situation is encountered, or even suspected, the remedy is to either lower the level of acceptable error or to breed several more kittens than would otherwise be necessary.


NUMBER OF KITTENS REQUIRED TO REDUCE THE ERROR PERCENTAGE TO BELOW A CERTAIN VALUE
(e.g. below the 5 or 1 per cent)

No. of Kittens	A	B	C
1	50	75	88
2	25	56	78
3	12.5	42	71
4	6.3	32	66
5	3.1	24	62
6	1.5	18	59
7	0.8	13	57
8	0.4	10	55
9	0.2	7.5	54
10	0.1	5.6	53
11	-	4.2	52
12	-	3.2	52
13	-	2.4	51
14	-	1.8	51
15	-	1.3	51
16	-	1.0	51
17	-	0.7	50
18	-	0.6	50
19	-	0.4	50
20	-	0.3	50

The situation may arise that none of the above techniques if test mating can be carried out. N this event, the elimination will have to rely upon selective culling, All affected animals should be banished from the breeding pen, together with their parents and sibs as far as this is consistent with the overall breeding plan. Familial selection is more efficient than individual selection. The appearance of a single affected kitten means that each parent is a heterozygote and two0thirds of the sibs will be potential heterozygotes. These are the facts to be borne I n mind in coming to a decision whether or nut to test mate or how ruthlessly to cull.

With polygenic heredity, the problem is that of detecting those animals which have a high propensity to produce anomalous kittens. Test mating is riled out in any simple sense and even with the determination of a high propensity for an individual means being wise after the event, If action is taken, it means being drastic because all of the healthy offspring will be potential “high producers”, however excellent they may be in other respects. It is a question of balancing the quality of the individual offspring against the chances of passing on of the anomaly.

There are two main types of anomaly with polygenic heredity, The first is that where the severity of the anomaly is variable and the severity is determined by the polygenes, This implies that culling if the most affected animals will bring about a gradual improvement. The extent of the improvement and the rate at which it occurs will depend on the level of culling. In general, the more ruthless the culling, the greater the relative improvement. There are various complicating factors, of course, of which the most important is that certain of the mildly affected animals (which are not culled) will be capable of producing severely affected offspring. Against this will be the fact that the average level of severity should decline per generation of selection.

The second type of polygenic trait is where the anomaly is due to a threshold effect. Despite the underlying polygenic inheritance, there is no real inter-grading as formerly, the animals are either normal or abnormal. The degree of abnormality may vary and this may be polygenically determined but the normals are, to all intents, fully normal in appearance. Test matings cannot be easily performed and the only remedy is that of selective culling of abnormals and, as far as practical, all those individuals with a high propensity to produce affected kittens.

To be really effective, the amount of selective culling should be ruthless. Ideally, once an anomaly has been assessed as genetic, no further young should be bred form either parent, none of the sibs should be used for breeding (regardless if their apparent healthiness or excellence), and the culling should extend into their immediate collateral relatives. In other words, a clean sweep is necessary. Doubtless, this is counsel of perfection and intolerably drastic, However, if the culling is less than this, a price must be paid in terms of breeding a small proportion of affected animals in future generations.