New roles for an old cyclin in control of cell cycle entry and cell size
Amanda Brambila, Beth E. Prichard, Jerry T. DeWitt, Douglas R. Kellogg
Abstract
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Amanda Brambila, Beth E. Prichard, Jerry T. DeWitt, Douglas R. Kellogg
Abstract
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Abstract Entry into the cell cycle in late G1 phase occurs only when sufficient growth has occurred. In budding yeast, a cyclin called Cln3 is thought to link cell cycle entry to cell growth. Cln3 accumulates during growth in early G1 phase and eventually triggers accumulation of late G1 phase cyclins that drive cell cycle entry. All current models for cell cycle entry assume that expression of late G1 phase cyclins is initiated at the transcriptional level. Current models also assume that the sole function of Cln3 in cell cycle entry is to promote transcription of late G1 phase cyclins, and that Cln3 works solely in G1 phase. Here, we show that cell cycle-dependent expression of late G1 phase cyclins does not require cell cycle-dependent transcription. Moreover, Cln3 can influence accumulation of late G1 phase cyclin proteins via post-transcriptional mechanisms. Finally, we show that Cln3 has functions in mitosis that strongly influence cell size. Together, these discoveries reveal surprising new functions for Cln3 that challenge current models for control of cell cycle entry and cell size.
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Abstract Entry into the cell cycle in late G1 phase occurs only when sufficient growth has occurred. In budding yeast, a cyclin called Cln3 is thought to link cell cycle entry to cell growth. Cln3 accumulates during growth in early G1 phase and eventually triggers accumulation of late G1 phase cyclins that drive cell cycle entry. All current models for cell cycle entry assume that expression of late G1 phase cyclins is initiated at the transcriptional level. Current models also assume that the sole function of Cln3 in cell cycle entry is to promote transcription of late G1 phase cyclins, and that Cln3 works solely in G1 phase. Here, we show that cell cycle-dependent expression of late G1 phase cyclins does not require cell cycle-dependent transcription. Moreover, Cln3 can influence accumulation of late G1 phase cyclin proteins via post-transcriptional mechanisms. Finally, we show that Cln3 has functions in mitosis that strongly influence cell size. Together, these discoveries reveal surprising new functions for Cln3 that challenge current models for control of cell cycle entry and cell size.
Key concepts: Cell cycle, Cyclin, Cell biology, Biology, Cyclin A, Mitosis, Cell Cycle Protein, Cell growth