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The cell cycle controls spindle architecture in Arabidopsis by modulating the augmin pathway

ABSTRACT: To ensure an even segregation of chromosomes during somatic cell division, eukaryotes rely on specific microtubule structures called mitotic spindles. There are however striking differences in overall spindle organization among eukaryotic super groups, and in particular little is known about how spindle architecture is determined in plants. As a foundation for our work, we have measured prime characteristics of Arabidopsis mitotic spindles and built a three-dimensional dynamic model of the Arabidopsis mitotic spindle using Cytosim. Next, we identified the cell-cycle regulator CYCLIN-DEPENDENT KINASE B1 (CDKB1) together with its cyclin partner CYCB3;1 as key regulators of spindle shape and organization in Arabidopsis. Loss of CDKB1 function resulted in a high number of astral microtubules that are normally absent from plant spindles, as opposed to animal ones. We identified an augmin complex member, ENDOSPERM DEFECTIVE1 (EDE1), as a substrate of the CDKB1;1-CYCB3;1 complex. A non-phosphorylatable mutant of EDE1 displayed spindles with extended pole-to-pole distance, resembling the phenotypes of cycb3;1 and cdkb1 mutants, and the mutated EDE1 associated less efficiently with spindle microtubules. Consistently, reducing the level of augmin in Cytosim simulations largely recapitulated the spindle phenotypes observed in cycb3;1 and cdkb1 mutants. Our results emphasize the importance of cell cycle-dependent phospho-control of the mitotic spindle in plant cells. They also support the validity of our computational model as a framework for the exploration of mechanisms controlling the organization of plant spindles

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)

TISSUE(S): Plant Cell

SUBMITTER: Sara Christina Stolze

LAB HEAD: Hirofumi Nakagami

PROVIDER: PXD046697 | Pride | 2024-08-27

REPOSITORIES: Pride

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			Action	DRS
	220315_220124_AS_MaMo_PRM_03_1.raw	Raw
	220315_220124_AS_MaMo_PRM_03_2.raw	Raw
	220315_220124_AS_MaMo_PRM_03_3.raw	Raw
	220315_220124_AS_MaMo_PRM_08_1.raw	Raw
	220315_220124_AS_MaMo_PRM_08_2.raw	Raw

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Project description:This model is from the article: A dynamical model of the spindle position checkpoint Ayse Koca Caydasi, Maiko Lohel, Gerd Grünert, Peter Dittrich, Gislene Pereira, Bashar Ibrahim Molecular Systems Biology 2012; 582 doi: 10.1038/msb.2012.15 Abstract: The orientation of the mitotic spindle with respect to the polarity axis is crucial for the accuracy of asymmetric cell division. In budding yeast, a surveillance mechanism called the spindle position checkpoint (SPOC) prevents exit from mitosis when the mitotic spindle fails to align along the mother-to-daughter polarity axis. SPOC arrest relies upon inhibition of the GTPase Tem1 by the GTPase-activating protein (GAP) complex Bfa1–Bub2. Importantly, reactions signaling mitotic exit take place at yeast centrosomes (named spindle pole bodies, SPBs) and the GAP complex also promotes SPB localization of Tem1. Yet, whether the regulation of Tem1 by Bfa1–Bub2 takes place only at the SPBs remains elusive. Here, we present a quantitative analysis of Bfa1–Bub2 and Tem1 localization at the SPBs. Based on the measured SPB-bound protein levels, we introduce a dynamical model of the SPOC that describes the regulation of Bfa1 and Tem1. Our model suggests that Bfa1 interacts with Tem1 in the cytoplasm as well as at the SPBs to provide efficient Tem1 inhibition. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

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The cell cycle controls spindle architecture in Arabidopsis by modulating the augmin pathway

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