Journal
SCIENCE ADVANCES
Volume 8, Issue 18, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abm4086
Keywords
-
Categories
Funding
- Agencia Estatal de Investigacion Spain [PGC2018-096597-B-I00]
- Agencia de Gestio d'Ajuts Universitaris i de Recerca Catalonia [2014FI_B 00074]
Ask authors/readers for more resources
Cells maintain their size to maximize fitness and survival. In budding yeast cells, a sizer mechanism regulates cell cycle entry. This study reveals that intertwined APC and SCF degradation machineries, along with specific adaptor proteins, drive cyclic accumulation of G(1) Cdk in the nucleus, which is important for cell cycle progression.
Cells maintain their size within limits over successive generations to maximize fitness and survival. Sizer, timer, and adder behaviors have been proposed as possible alternatives to coordinate growth and cell cycle progression. Regarding budding yeast cells, a sizer mechanism is thought to rule cell cycle entry at Start. However, while many proteins controlling the size of these cells have been identified, the mechanistic framework in which they participate to achieve cell size homeostasis is not understood. We show here that intertwined APC and SCF degradation machineries with specific adaptor proteins drive cyclic accumulation of the G(1) Cdk in the nucleus, reaching maximal levels at Start. The mechanism incorporates Mad3, a centromeric-signaling protein that subordinates G(1) progression to the previous mitosis as a memory factor. This alternating-degradation device displays the properties of a timer and, together with the sizer device, would constitute a key determinant of cell cycle entry.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available