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Transcriptional and post‐transcriptional regulation of histone variant H2A.Z during sea urchin development
Author(s) -
Hajdu Mihai,
Calle Jasmine,
Puno Andrea,
Haruna Aminat,
ArenasMena César
Publication year - 2016
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/dgd.12329
Subject(s) - biology , chromatin , transcriptional regulation , histone , strongylocentrotus purpuratus , chromatin immunoprecipitation , regulation of gene expression , genetics , transcription (linguistics) , gene , microbiology and biotechnology , transcription factor , gene expression , promoter , linguistics , philosophy
Histone variant H2A.Z promotes chromatin accessibility at transcriptional regulatory elements and is developmentally regulated in metazoans. We characterize the transcriptional and post‐transcriptional regulation of H2A.Z in the purple sea urchin Strongylocentrotus purpuratus . H2A.Z depletion by antisense translation‐blocking morpholino oligonucleotides during early development causes developmental collapse, in agreement with its previously demonstrated general role in transcriptional multipotency. During H2A.Z peak expression in 24‐h embryos, endogenous H2A.Z 3′ UTR sequences stabilize GFP mRNA s relative to those with SV 40 3′ UTR sequences, although the 3′ UTR of H2A.Z does not determine the spatial distribution of H2A.Z transcripts during embryonic and postembryonic development. We elaborated an H2A.Z:: GFP BAC reporter that reproduces embryonic H2A.Z expression. Genome‐wide chromatin accessibility analysis using ATAC ‐seq revealed a cis‐ regulatory module ( CRM ) that, when deleted, causes a significant decline of the H2A.Z reporter expression. In addition, the mutation of a Sox transcription factor binding site motif and, more strongly, of a Myb motif cause significant decline of reporter gene expression. Our results suggest that an undetermined Myb‐family transcription factor controls the transcriptional regulation of H2A.Z .