AI Article Synopsis

  • The Rlm1 transcription factor is influenced by the cell wall integrity pathway and plays a key role in regulating cell division.
  • An Δ mutant with abnormal cell grouping displays a precocious transition from G to S phase compared to normal cells, leading to the introduction of the CW/START checkpoint.
  • The phenotype of Δ satellite daughter cells is reversible under certain conditions, and the effect of Rlm1 may relate to the organization of the actin cytoskeleton, crucial for proper cell division progression.

Article Abstract

The Rlm1 transcription factor is a target of the cell wall integrity pathway. We report that an Δ mutant grown on a nonfermentable carbon source at low osmolarity forms cell groups in which a mother cell is surrounded by smaller "satellite-daughter" cells. Mother cells in these groups progressed through repeated rounds of cell division with normal rates of bud growth and genetic stability; however, these cells underwent precocious START relative to wild-type mothers. Thus, once activated, Rlm1 delays the transition from G to S, a mechanism we term the cell wall/START (CW/START) checkpoint. The Δ satellite-cell phenotype is suppressed by deletion of either , which encodes the kinase that activates Rlm1, or , which is also activated by Slt2; suggesting that Slt2 can have opposing roles in regulating the START transition. Consistent with an Rlm1-dependent CW/START checkpoint, Δ satellite daughters were unable to grow or divide further even after transfer to rich medium, but UV irradiation in G could partially rescue Δ satellite daughters in the next division. Indeed, after cytokinesis, these satellite daughters shrank rapidly, displayed amorphous actin staining, and became more permeable. As a working hypothesis, we propose that duplication of an "actin-organizing center" in late G may be required both to progress through START and to reestablish the actin cytoskeleton in daughter cells.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560798PMC
http://dx.doi.org/10.1534/genetics.117.204206DOI Listing

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