Search bioRxivSearch

Biology subjects

Allard, C. A. H.

Publications and source records attributed to Allard, C. A. H..

2 recordsLinked to original sources

A size-invariant bud-length timer enables robustness in yeast cell size control

Cell populations across nearly all forms of life generally maintain a characteristic cell type-dependent size, but how size control is achieved has been a long-standing question. Prior work has uncovered diverse size control strategies operating at distinct cell cycle stages, but it is unclear how these numerous pathways are integrated to provide robust, systems-level cell size control for any organism. Here, we probe cell growth and size control in budding yeast that can be reversibly blocked from bud initiation. While blocked, cells continue to grow isotropically, increasing their volume by more than an order of magnitude over unperturbed cells. Upon release, these giant yeast resume budding and the population returns to its initial volume distribution within a few cell division cycles. Size control under these conditions does not require an explicit molecular size sensor. Instead, our observations are consistent with a size-invariant bud growth timer specifying the duration of S/G2/M to limit daughter cell size.

cell biology

Cell size-dependent regulation of Wee1 localization by Cdr2 cortical nodes

Cell size control requires mechanisms that link cell growth with Cdk1 activity. In fission yeast, the protein kinase Cdr2 forms cortical nodes that include the Cdk1 inhibitor Wee1, along with the Wee1-inhibitory kinase Cdr1. We investigated how nodes inhibit Wee1 during cell growth. Biochemical fractionation revealed that Cdr2 nodes were megadalton structures enriched for activated Cdr2, which increases in level during interphase growth. In live-cell TIRF movies, Cdr2 and Cdr1 remained constant at nodes over time, but Wee1 localized to nodes in short bursts. Recruitment of Wee1 to nodes required Cdr2 kinase activity and the noncatalytic N-terminus of Wee1. Bursts of Wee1 localization to nodes increased 20-fold as cells doubled in size throughout G2. Size-dependent signaling was due in part to the Cdr2 inhibitor Pom1, which suppressed Wee1 node bursts in small cells. Thus, increasing Cdr2 activity during cell growth promotes Wee1 localization to nodes, where inhibitory phosphorylation of Wee1 by Cdr1 and Cdr2 kinases promotes mitotic entry.\n\nSummaryCells turn off the mitotic inhibitor Wee1 to enter into mitosis. This study shows how cell growth progressively inhibits fission yeast Wee1 through dynamic bursts of localization to cortical node structures that contain Wee1 inhibitory kinases.

cell biology