The University of Colorado School of Medicine's Richard Davis et al. this week report known and novel small RNA classes in the parasitic nematode Ascaris sum, which they've compared with with known small RNAs of Caenorhabditis elegans. Overall, the team found that "piRNAs, Piwi-clade Argonautes, and other proteins associated with the piRNA pathway have been lost in Ascaris," and that in this particular nematode, miRNAs "are synthesized immediately after fertilization in utero, before pronuclear fusion, and before the first cleavage of the zygote."
Researchers at Australia's Garvan Institute of Medical Research show in a Genome Research paper published online in advance this week that "acetylation of H2A.Z is a key epigenetic modification associated with gene deregulation and epigenetic remodeling in cancer." In its investigation, the team found that acetylated H2A.Z is "only localized at the TSSs [transcription start sites] of active genes" and, further, that "gene deregulation in cancer is also associated with a reorganization of [acetylated]H2A.Z and H2A.Z nucleosome occupancy across the promoter region and TSS of genes." Thus, the authors say that their work shows for the first time that H2A.Z acetylation "is a key modification associated with gene activity in normal cells and epigenetic gene deregulation in tumorigenesis."
In another Genome Research paper recently published online, investigators at the UC Davis School of Medicine show that genomic regions marked by cell line-specific partially methylated domains contain genes that are expressed in a tissue-specific manner, such that the partially methylated domains are a "mark of repressed transcription." The team also shows that certain autism candidate genes are enriched within partially methylated domains, of which it observed the largest in "SH-SY5Y cells, [which] marked a 10 Mb [megabase] cluster of cadherin genes with strong genetic association to autism." The team suggests that further "large-scale methylation domain maps could be relevant to interpreting and directing future investigations into the elusive etiology of autism."
Elsewhere in Genome Research, University of Washington's James Thomas and Sean Schneider write about the forces that may "have driven the number and diversity of tandem zinc finger genes" and, in particular, Thomas and Schneider discuss their support for a "host-pathogen model for tandem ZF gene evolution, in which new LTR [long terminal repeat] retroelement challenges drive duplication and divergence of host tandem ZF genes."
[Editors' note: An earlier version of this post incorrectly identified the journal in which the third and fourth papers were published. Daily Scan regrets the error.]