AI Article Synopsis

  • Meiosis is a specialized cell division process that reduces chromosome number and is crucial for the formation of gametes in plants like Arabidopsis, where it transitions to gametophyte development through translation inhibition mechanisms involving TDM1 and SMG7.
  • Mutants lacking these mechanisms experience abnormal nuclear divisions due to the inability to downregulate cyclin-dependent kinases, resulting in the failure to form tetrads.
  • A suppressor screen identified mutation in CDKD;3, which alleviates these meiotic defects by preventing aberrant divisions and promoting the formation of functional microspores, indicating its complex role in cell cycle regulation beyond just activating CDKA;1.

Article Abstract

Meiosis is a specialized cell division that halves the number of chromosomes in two consecutive rounds of chromosome segregation. In angiosperm plants is meiosis followed by mitotic divisions to form rudimentary haploid gametophytes. In Arabidopsis, termination of meiosis and transition to gametophytic development are governed by TDM1 and SMG7 that mediate inhibition of translation. Mutants deficient in this mechanism do not form tetrads but instead undergo multiple cycles of aberrant nuclear divisions that are likely caused by the failure to downregulate cyclin dependent kinases during meiotic exit. A suppressor screen to identify genes that contribute to meiotic exit uncovered a mutation in cyclin-dependent kinase D;3 (CDKD;3) that alleviates meiotic defects in deficient plants. The CDKD;3 deficiency prevents aberrant meiotic divisions observed in mutants or delays their onset after initiation of cytokinesis, which permits formation of functional microspores. Although CDKD;3 acts as an activator of cyclin-dependent kinase A;1 (CDKA;1), the main cyclin dependent kinase that regulates meiosis, mutation appears to promote meiotic exit independently of CDKA;1. Furthermore, analysis of CDKD;3 interactome revealed enrichment for proteins implicated in cytokinesis, suggesting a more complex function of CDKD;3 in cell cycle regulation.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9986724PMC
http://dx.doi.org/10.1002/pld3.477DOI Listing

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