ABSTRACT
A gene does not have the same effect (value) in all individuals in which it occurs. The effect of a particular allele may differ according to the identity of the other allele at the same locus (known as dominance) and also depends on which alleles are found at other loci (epistasis). Dominance and epistasis are nonlinear genetic effects that mask the expression of the additive genetic variation. The variation within a herd can be partitioned into environmental and additive genetic variance. An animal’s breeding value is its additive genetic value, and its variance constitutes the additive genetic variance. The heritability (h2) of a trait is that proportion of the total variance that is due to additive genetic variance, and is used to predict the probable response to selection for quantitative characters.[1]
Mendelian Inheritance in Goats
There are several genetic disorders associated with characteristics found in goats, which are caused by single genes. These are summarized in Tables 1 and 2. The autosomal dominant polled gene P, causes hornlessness and its recessive ( p) causes sexual abnormality in goats.[1,2] The absence of wattles and the absence of ears have been shown to be recessive characters.[2] Coat color may be important
in skin and hair production (e.g., in the Red Sokoto and Cashmere goats). The order of dominance in coat color is white, red, fawn or chamois, and black, and the wild-type face pattern found in Toggenburgs is dominant to the reversed pattern known as badger face.[3]
Traditionally, genetic crosses have been used to determine the presence of alleles that code for a particular phenotype. In qualitative inheritance, only one pair of genes or a single locus is involved. Most inheritance involves multiple genes or quantitative trait loci (QTL).[4] Recent advances in molecular genetic analyses-restriction fragment length polymorphism analyses (RFLP), randomly amplified polymorphic DNA (RAPD), simple sequence repeat (SSR) microsatellites, amplification fragment length polymorphism (AFLP), and single nucleotide polymorphism (SNP) analyses-have allowed the development of a variety of DNA-based markers. With sufficiently dense genetic maps, entire genomes can be scanned for genes associated with QTL.[5] Once a QTL has been identified, populations can be tested quickly and easily for the frequency of alleles and associated phenotypes.
