English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Background  Polycomb-group (PcG) and trithorax-group (trxG) proteins regulate histone methylation to establish repressive and active chromatin configurations at target loci, respectively. These chromatin configurations are passed on from mother to daughter cells, thereby causing heritable changes in gene expression. The activities of PcG and trxG proteins are regulated by a special class of proteins known as Enhancers of trithorax and Polycomb (ETP). The  Drosophila  gene  Additional sex combs  ( Asx ) encodes an ETP protein and mutations in  Asx  enhance both PcG and trxG mutant phenotypes. The mouse and human genomes each contain three  Asx  homologues,  Asx-like 1 ,  2 , and  3 . In order to understand the functions of mammalian Asx-like (Asxl) proteins, we generated an  Asxl2  mutant mouse from a gene-trap ES cell line.    Methodology/Principal Findings  We show that the  Asxl2  gene trap is expressed at high levels in specific tissues including the heart, the axial skeleton, the neocortex, the retina, spermatogonia and developing oocytes. The gene trap mutation is partially embryonic lethal and approximately half of homozygous animals die before birth. Homozygotes that survive embryogenesis are significantly smaller than controls and have a shortened life span.  Asxl2 −/−   mice display both posterior transformations and anterior transformation in the axial skeleton, suggesting that the loss of  Asxl2  disrupts the activities of both PcG and trxG proteins. The PcG-associated histone modification, trimethylation of histone H3 lysine 27, is reduced in  Asxl2 −/−   heart. Necropsy and histological analysis show that mutant mice have enlarged hearts and may have impaired heart function.    Conclusions/Significance  Our results suggest that murine  Asxl2  has conserved ETP function and plays dual roles in the promotion of PcG and trxG activity. We have also revealed an unexpected role for  Asxl2  in the heart, suggesting that the PcG/trxG system may be involved in the regulation of cardiac function.

Functional Conservation of Asxl2, a Murine Homolog for the Drosophila Enhancer of Trithorax and Polycomb Group Gene Asx