{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sawant OB"],"funding":["BLRD VA","NEI NIH HHS","National Eye Institute","Knights Templar Eye Foundation","National Institutes of Health","U.S. Department of Veterans Affairs"],"pagination":["8745-8758"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6662963"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["33(8)"],"pubmed_abstract":["A single pool of multipotent retinal progenitor cells give rise to the diverse cell types within the mammalian retina. Such cellular diversity is due to precise control of various cellular processes like cell specification, proliferation, differentiation, and maturation. Circadian clock genes can control the expression of key regulators of cell cycle progression and therefore can synchronize the cell cycle state of a heterogeneous population of cells. Here we show that the protein encoded by the circadian clock gene brain and muscle arnt-like protein-1 (<i>Bmal1</i>) is expressed in the embryonic retina and is required to regulate the timing of cell cycle exit. Accordingly, loss of <i>Bmal1</i> during retinal neurogenesis results in increased S-phase entry and delayed cell cycle exit. Disr"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["The circadian clock gene <i>Bmal1</i> is required to control the timing of retinal neurogenesis and lamination of Muller glia in the mouse retina."],"pmcid":["PMC6662963"],"funding_grant_id":["P30 EY025585","IK6 BX005233","KTEF1806","R01 EY032029","P30‐EY025585","R01 EY027077"],"pubmed_authors":["Zucaro OF","Rao S","Yu M","Sawant OB","Fuller RD","Jidigam VK","Peachey NS","Kpegba C"],"additional_accession":[]},"is_claimable":false,"name":"The circadian clock gene <i>Bmal1</i> is required to control the timing of retinal neurogenesis and lamination of Muller glia in the mouse retina.","description":"A single pool of multipotent retinal progenitor cells give rise to the diverse cell types within the mammalian retina. Such cellular diversity is due to precise control of various cellular processes like cell specification, proliferation, differentiation, and maturation. Circadian clock genes can control the expression of key regulators of cell cycle progression and therefore can synchronize the cell cycle state of a heterogeneous population of cells. Here we show that the protein encoded by the circadian clock gene brain and muscle arnt-like protein-1 (<i>Bmal1</i>) is expressed in the embryonic retina and is required to regulate the timing of cell cycle exit. Accordingly, loss of <i>Bmal1</i> during retinal neurogenesis results in increased S-phase entry and delayed cell cycle exit. Disr","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Aug","modification":"2025-05-29T20:47:51.783Z","creation":"2025-05-29T20:47:51.783Z"},"accession":"S-EPMC6662963","cross_references":{"pubmed":["31002540"],"doi":["10.1096/fj.201801832RR","10.1096/fj.201801832rr"]}}