In:
Genes & Development, Cold Spring Harbor Laboratory, Vol. 35, No. 13-14 ( 2021-07-01), p. 1055-1070
Abstract:
The dosage compensation complex (DCC) of Drosophila identifies its X-chromosomal binding sites with exquisite selectivity. The principles that assure this vital targeting are known from the D. melanogaster model: DCC-intrinsic specificity of DNA binding, cooperativity with the CLAMP protein, and noncoding roX2 RNA transcribed from the X chromosome. We found that in D. virilis , a species separated from melanogaster by 40 million years of evolution, all principles are active but contribute differently to X specificity. In melanogaster , the DCC subunit MSL2 evolved intrinsic DNA-binding selectivity for rare PionX sites, which mark the X chromosome. In virilis , PionX motifs are abundant and not X-enriched. Accordingly, MSL2 lacks specific recognition. Here, roX2 RNA plays a more instructive role, counteracting a nonproductive interaction of CLAMP and modulating DCC binding selectivity. Remarkably, roX2 triggers a stable chromatin binding mode characteristic of DCC. Evidently, X-specific regulation is achieved by divergent evolution of protein, DNA, and RNA components.
Type of Medium:
Online Resource
ISSN:
0890-9369
,
1549-5477
DOI:
10.1101/gad.348411.121
Language:
English
Publisher:
Cold Spring Harbor Laboratory
Publication Date:
2021
detail.hit.zdb_id:
1467414-2
SSG:
12
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