BMB Reports | |
Clustered LAG-1 binding sites in lag-1/CSL are involved in regulating lag-1 expression during lin-12/Notch-dependent cell-fate specification | |
Vit Na Choi^11  | |
[1] Department of Molecular Bioscience, College of Biomedical Science, Kangwon National University, Chuncheon 200-701, Korea^1 | |
关键词: Anchor cell/ventral uterine precursor cell; | |
DOI : | |
学科分类:生物化学/生物物理 | |
来源: Korean Society for Biochemistry and Molecular Biology | |
【 摘 要 】
The cell-fate specification of the anchor cell (AC) and a ventral uterine precursor cell (VU) in Caenorhabditis elegans is initiated by a stochastic interaction between LIN-12/Notch receptor and LAG-2/Delta ligand in two neighboring Z1.ppp and Z4.aaa cells. Both cells express lin-12 and lag-2 before specification, and a small difference in LIN-12 activity leads to the exclusive expressions of lin-12 in VU and lag-2 in the AC, through a feedback mechanism of unknown nature. Here we show that the expression pattern of lag-1/CSL, a transcriptional repressor itself that turns into an activator upon binding of the intracellular domain of Notch, overlaps with that of lin-12. Site-directed mutagenesis of LAG-1 binding sites in lag-1 maintains its expression in the AC, and eliminates it in the VU. Thus, AC/VU cell-fate specification appears to involve direct regulation oflag-1 expression by the LAG-1 protein, activating its transcription in VU cells, but repressing it in the AC.
【 授权许可】
Unknown
【 预 览 】
Files | Size | Format | View |
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RO201910256509990ZK.pdf | 1146KB | download |