Background: The ways in which cells set the size of intracellular structures is an important but largely unsolved problem [1]. Early embryonic divisions pose special problems in this regard. Many checkpoints common in somatic cells are missing from these divisions, which are characterized by rapid reductions in cell size and short cell cycles [2]. Embryonic cells must therefore possess simple and robust mechanisms that allow the size of many of their intracellular structures to rapidly scale with cell size.
Results: Here, we study the mechanism by which one structure, the centrosome, scales in size during the early embryonic divisions of C. elegans. We show that centrosome size is directly related to cell size and is independent of lineage. Two findings suggest that the total amount of maternally supplied centrosome proteins could limit centrosome size. First, the combined volume of all centrosomes formed at any one time in the developing embryo is constant. Second, the total volume of centrosomes in any one cell is independent of centrosome number. By increasing the amount of centrosome proteins in the cell, we provide evidence that one component that limits centrosome size is the conserved pericentriolar material protein SPD-2 [3], which we show binds to and targets polo-like kinase 1 [3, 4] to centrosomes.
Conclusions: We propose a limiting component hypothesis, in which the volume of the cell sets centrosome size by limiting the total amount of centrosome components. This idea could be a general mechanism for setting the size of intracellular organelles during development.
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http://dx.doi.org/10.1016/j.cub.2011.06.002 | DOI Listing |
Methods Mol Biol
December 2024
Graduate School of Life Science, Hokkaido University, Sapporo, Japan.
Drastic changes in chromosome number and cellular contents upon ploidy alterations profoundly affect the stability of mitotic regulation in different biological and pathological processes. Isogenic ploidy series of somatic cell lines are useful for studying the effects of ploidy differences on mitotic regulation at cellular and molecular levels. This chapter describes experimental procedures using isogenic human HAP1 cell lines that cover haploid, diploid, and tetraploid states.
View Article and Find Full Text PDFMethods Mol Biol
December 2024
Université Paris Cité, CNRS, Institut Jacques Monod, Paris, France.
FASEB J
November 2024
Department of Biological Sciences, Seoul National University, Seoul, Korea.
bioRxiv
October 2024
Department of Ecology, Behavior, and Evolution, School of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
Intrinsic reproductive isolation occurs when genetic differences between populations disrupt the development of hybrid organisms, preventing gene flow and enforcing speciation. While prior studies have examined the genetic origins of hybrid incompatibility, the effects of incompatible factors on development remain poorly understood. Here, we investigate the mechanistic basis of hybrid incompatibility in nematodes by capitalizing on the ability of females to produce embryos after mating with males from several other species.
View Article and Find Full Text PDFOpen Biol
October 2024
Graduate School of Life Science, Hokkaido University, Kita 21, Nishi 11, Kita-Ku , Sapporo 001-0021, Japan.
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