X Chromosome Inactivation 

Samaah Zohair The X-inactivation is in the sex chromosome only, I don't think this concept can be applied to autosomal chromosomes. Sorry for riding on your comment😅

no

Unfortunately, I'm not a cat geneticist, so I'm not sure of the answer to your question. However, I can add that the genetic basis of traits (like coat color) is not always simple. It might be that white spots is controlled by a gene not found on either X chromosome and so that white spots would having nothing to do with X-chromosome inactivation. Again, I don't know that this is a correct explanation, but its basis is genetically plausible.

@@JosephRoss ah okay thanks a lot for your time I might need to search more .

I know that this has been a while back, but this is because of the concept of "Epistasis": it occurs when one gene affects the phenotypic expression of a second gene. This frequently occurs in the expression of pigmentation. One gene turns on (or off) the production of pigment, while a second gene controls either the amount of pigment produced or the color of the pigment. If the first gene codes for no pigment, then the expression of the second gene has no effect, regardless of the kind of pigmentation it encodes. Epistasis occurs in the pigmentation of fur in mice. One gene codes for the presence or absence of pigmentation. A second gene codes for the color of pigmentation, black or brown. Thus, C and c represent the alleles for the presence and absence of color, and B and b represent the alleles for black and brown pigments. As the allele notation indicates, both genes are expressed by the complete dominance inheritance pattern. The phenotypic expressions of CCBB, CCBb, CcBB, and CcBb are all black, and the expressions of CCbb and Ccbb are both brown. However, whenever cc is inherited, no pigment is produced and the fur is white regardless of the color encoded by the B allele. This process is similar in Calico Cats.

From wiki: "Turner syndrome has distinct features due to the lack of pseudoautosomal regions, which are typically spared from X-inactivation."

Possibly for many reasons, but likely at least two: even on the inactive X, some genes escape silencing, which can cause gene dosage problems; prior to XCI, having the incorrect number of chromosomes could also cause developmental/physiological issues.

@@JosephRoss Sir, does that mean different people having the same type of sex chromosomal(X linked) defect will present the symptoms differently because the extent of gene silencing is different in every individual