Detection of the responsible expansions is complicated in both cases because of the extremely variable length of the expanded alleles, which can contain even several thousands of repeats in both disorders.
Intragenic duplication and divergence might be the major driving force responsible for expansion of novel snoRNAs in the chicken genome.
As tumours are clonally derived (Nowell, 1976), it would be expected that an abnormality responsible for expansion of the neoplasm would be present throughout – this was not observed in these samples.
As IL-2 is responsible for expansion and differentiation of T regulatory cells (Tregs) and also activation-induced cell death, autoimmunity arises in both IL-2−/− and CD25−/− strains [ 6, 8, 10].
Our results suggest that the chicken is a good model for the prediction of functional snoRNAs, and that intragenic duplication and divergence might be the major driving forces responsible for expansion of novel snoRNA genes in the chicken genome.
These findings indicate that heteromorphism can evolve without chromosomal translocations, are consistent with the accumulation of transposable elements and repeated sequences in nonrecombining regions being responsible for expansion of MSY, and may explain why plant Y chromosomes tend to be larger than their X counterparts.
With known inducers of Pea3, such as FGF8/3 and Wnt1, not being expressed in the pioneer pool, work is currently underway to identify the signal, induced by HGF/Met in pioneer neurons, that is responsible for expansion of the Pea3 expression domain, not only laterally, within the Met-expressing CM MN pool, but also to Met-negative anterior MNs.
It is argued that human activities have been largely responsible for expansions and contractions of silver fir populations.
HD is an autosomal dominant disease caused by a mutation in the gene encoding the huntingtin protein (htt); this mutation is responsible for abnormal expansion of a trinucleotide CAG repeat encoding polyglutamine tract expansion in the N terminus of htt [ 64].
Given that RuvAB-dependent replication fork reversal was not responsible for repeat expansion in a rep mutant, we continued to look for other activities that might promote or inhibit repeat expansion.
