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Updated: Aug 23, 2026

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Published on: November 7, 2006
Regulation of G2/M progression by the STE mitogen-activated protein kinase pathway in budding yeast filamentous
1Center for Molecular Oncology and Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, Illinois 60637, USA.
Abstract:
Inoculation of diploid budding yeast onto nitrogen-poor agar media stimulates a MAPK pathway to promote filamentous growth. Characteristics of filamentous cells include a specific pattern of gene expression, elongated cell shape, polar budding pattern, persistent attachment to the mother cell, and a distinct cell cycle characterized by cell size control at G2/M. Although a requirement for MAPK signaling in filamentous gene expression is well established, the role of this pathway in the regulation of morphogenesis and the cell cycle remains obscure. We find that ectopic activation of the MAPK signal pathway induces a cell cycle shift to G2/M coordinately with other changes characteristic of filamentous growth. These effects are abrogated by overexpression of the yeast mitotic cyclins Clb1 and Clb2. In turn, yeast deficient for Clb2 or carrying cdc28-1N, an allele of CDK defective for mitotic functions, display enhanced filamentous differentiation and supersensitivity to the MAPK signal. Importantly, activation of Swe1-mediated inhibitory phosphorylation of Thr-18 and/or Tyr-19 of Cdc28 is not required for the MAPK pathway to affect the G2/M delay. Mutants expressing a nonphosphorylatable mutant Cdc28 or deficient for Swe1 exhibit low-nitrogen-dependent filamentous growth and are further induced by an ectopic MAPK signal. We infer that the MAPK pathway promotes filamentous growth by a novel mechanism that inhibits mitotic cyclin/CDK complexes and thereby modulates cell shape, budding pattern, and cell-cell connections.
Insights
The MAPK pathway in yeast controls filamentous growth by delaying the cell cycle at G2/M. This pathway inhibits mitotic cyclin/CDK complexes, influencing cell shape and connections.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- Nitrogen-poor media induces filamentous growth in yeast via a MAPK pathway.
- Filamentous yeast exhibit distinct gene expression, cell shape, budding, and cell cycle control.
- The role of MAPK signaling in yeast morphogenesis and cell cycle regulation is not fully understood.
Purpose of the Study:
- To investigate the role of the MAPK pathway in regulating yeast cell cycle and morphogenesis during filamentous growth.
- To elucidate the molecular mechanisms by which MAPK signaling influences cell cycle progression and cell morphology.
Main Methods:
- Ectopic activation of the MAPK signal pathway in yeast.
- Overexpression of yeast mitotic cyclins Clb1 and Clb2.
- Analysis of yeast mutants deficient for Clb2 or carrying the cdc28-1N allele.
- Investigation of Swe1-mediated phosphorylation of Cdc28.
- Assessment of cell cycle progression and filamentous differentiation.
Main Results:
- Ectopic MAPK activation causes a G2/M cell cycle shift and filamentous characteristics.
- Overexpression of Clb1/Clb2 abrogates MAPK-induced cell cycle effects.
- Yeast deficient for Clb2 or with cdc28-1N show enhanced filamentous growth and MAPK sensitivity.
- MAPK pathway effects on G2/M delay are independent of Swe1-mediated Cdc28 phosphorylation.
- MAPK signaling inhibits mitotic cyclin/CDK complexes.
Conclusions:
- The MAPK pathway promotes yeast filamentous growth through a novel mechanism involving inhibition of mitotic cyclin/CDK complexes.
- This inhibition modulates yeast cell shape, budding pattern, and cell-cell connections.
- The findings provide new insights into cell cycle control and morphogenesis in response to environmental cues.
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