biostudies-literatureKohler RUniversity of LeipzigDeutsche ForschungsgemeinschaftRoland-Ernst-Stiftung6830-6849https://www.ebi.ac.uk/biostudies/studies/S-EPMC11229319biostudies-literatureUnknown52(12)A-MYB (MYBL1) is a transcription factor with a role in meiosis in spermatocytes. The related B-MYB protein is a key oncogene and a master regulator activating late cell cycle genes. To activate genes, B-MYB forms a complex with MuvB and is recruited indirectly to cell cycle genes homology region (CHR) promoter sites of target genes. Activation through the B-MYB-MuvB (MMB) complex is essential for successful mitosis. Here, we discover that A-MYB has a function in transcriptional regulation of the mitotic cell cycle and can substitute for B-MYB. Knockdown experiments in cells not related to spermatogenesis show that B-MYB loss alone merely delays cell cycle progression. Only dual knockdown of B-MYB and A-MYB causes G2/M cell cycle arrest, endoreduplication, and apoptosis. A-MYB can substitutNucleic acids researchA-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation.PMC1122931904/22424870812Kohler REngeland KfalseA-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation.A-MYB (MYBL1) is a transcription factor with a role in meiosis in spermatocytes. The related B-MYB protein is a key oncogene and a master regulator activating late cell cycle genes. To activate genes, B-MYB forms a complex with MuvB and is recruited indirectly to cell cycle genes homology region (CHR) promoter sites of target genes. Activation through the B-MYB-MuvB (MMB) complex is essential for successful mitosis. Here, we discover that A-MYB has a function in transcriptional regulation of the mitotic cell cycle and can substitute for B-MYB. Knockdown experiments in cells not related to spermatogenesis show that B-MYB loss alone merely delays cell cycle progression. Only dual knockdown of B-MYB and A-MYB causes G2/M cell cycle arrest, endoreduplication, and apoptosis. A-MYB can substitut2024-01-01T00:00:00Z2024 Jul2026-04-08T19:20:23.459Z2025-04-04T11:24:15.186ZS-EPMC112293193874734510.1093/nar/gkae370