is an exciting question that will have a large disease relevance. I think this is not so much about cytogenetic abnormalities but the general understanding which genetic modules are recombining, e.g. are compatible in terms of function, and which need to be tight together. Continue reading How we are reshuffling our genome
Ever since I heard 1976 about the Lyon hypothesis (described already in 1961 by Mary Frances Lyon) of X inactivation I wondered how this works on a molecular level – locking this chromosome in a separate nuclear compartment, condense it or encase it? Silencing a whole chromosome probably needs a concerted action of higher order DNA structure, histone code modification and primary sequence features. The last seems to be indeed relevant as C. elegans X has a target for gene expression repression by the dosage compensation complex – small rex motifs (X recruitment elements) ?CAGGGG and ?GTAATTG. The strength of DCC recruitment is correlated with rex motif number BUT rex motifs are not enriched on X – so certainly more features need to synergize for X repression. Yea, yea.