Faculty Opinions recommendation of Suspended animation in C. elegans requires the spindle checkpoint.

The orderly progression through the cell division cycle is of paramount importance to all organisms, as improper progression through the cycle could result in defects with grave consequences. Previously, our lab has shown that model eukaryotes such as Saccharomyces cerevisiae, Caenorhabditis elegans, and Danio rerio all retain high viability after prolonged arrest in a state of anoxia-induced suspended animation, implying that in such a state, progression through the cell division cycle is reversibly arrested in an orderly manner. Here, we show that S. cerevisiae (both wild-type and several cold-sensitive strains) and C. elegans embryos exhibit a dramatic decrease in viability that is associated with dysregulation of the cell cycle when exposed to low temperatures. Further, we find that when the yeast or worms are first transitioned into a state of anoxia-induced suspended animation before cold exposure, the associated cold-induced viability defects are largely abrogated. We present evidence that by imposing an anoxia-induced reversible arrest of the cell cycle, the cells are prevented from engaging in aberrant cell cycle events in the cold, thus allowing the organisms to avoid the lethality that would have occurred in a cold, oxygenated environment.

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Bacterial small RNAs and host epigenetic effectors of a transgenerational memory of pathogens in C. elegans.

10.1101/2021.03.26.437277 ◽

2021 ◽

Author(s):

Marcela E Legüe ◽

Blanca Aguila ◽

Bernardo Pollak ◽

Andrea Calixto

Keyword(s):

Quorum Sensing ◽

Small Rna ◽

Small Rnas ◽

Mechanisms Of Action ◽

Suspended Animation ◽

Rna Dynamics ◽

C Elegans ◽

Behavioral Adaptations ◽

Starting Point ◽

Pathogen Exposure

The inheritance of memories is adaptive for survival. Microbes interact with all organisms challenging their immunity and triggering behavioral adaptations. Some of these behaviors induced by bacteria can be inherited although the mechanisms of action are largely unexplored. In this work, we use C. elegans and its bacteria to study the transgenerational RNA dynamics of an interspecies crosstalk leading to a heritable behavior. Heritable responses to bacterial pathogens in the nematode include avoidance and pathogen-induced diapause (PIDF), a state of suspended animation to evade the pathogen threat. We identify a small RNA RsmY, involved in quorum sensing from P. aeruginosa as required for initiation of PIDF. Histone methyltransferase SET-18/SMYD3 is also needed for PIDF initiation in C. elegans. In contrast, SET-25/EHMT2 is necessary for the maintenance of the memory of pathogen exposure in the transgenerational lineage. This work can be a starting point to understanding microbiome-induced inheritance of acquired traits.

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Kinetochore-localized BUB-1/BUB-3 complex promotes anaphase onset in C. elegans

The Journal of Cell Biology ◽

10.1083/jcb.201412035 ◽

2015 ◽

Vol 209 (4) ◽

pp. 507-517 ◽

Cited By ~ 24

Author(s):

Taekyung Kim ◽

Mark W. Moyle ◽

Pablo Lara-Gonzalez ◽

Christian De Groot ◽

Karen Oegema ◽

...

Keyword(s):

Spindle Checkpoint ◽

Kinase Domain ◽

Mitotic Chromosomes ◽

Checkpoint Signaling ◽

C Elegans ◽

Anaphase Onset ◽

Checkpoint Pathway ◽

Chromosome Alignment ◽

Kinetochore Region

The conserved Bub1/Bub3 complex is recruited to the kinetochore region of mitotic chromosomes, where it initiates spindle checkpoint signaling and promotes chromosome alignment. Here we show that, in contrast to the expectation for a checkpoint pathway component, the BUB-1/BUB-3 complex promotes timely anaphase onset in Caenorhabditis elegans embryos. This activity of BUB-1/BUB-3 was independent of spindle checkpoint signaling but required kinetochore localization. BUB-1/BUB-3 inhibition equivalently delayed separase activation and other events occurring during mitotic exit. The anaphase promotion function required BUB-1’s kinase domain, but not its kinase activity, and this function was independent of the role of BUB-1/BUB-3 in chromosome alignment. These results reveal an unexpected role for the BUB-1/BUB-3 complex in promoting anaphase onset that is distinct from its well-studied functions in checkpoint signaling and chromosome alignment, and suggest a new mechanism contributing to the coordination of the metaphase-to-anaphase transition.

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PCH-2 collaborates with CMT-1 to proofread meiotic homolog interactions

10.1101/780254 ◽

2019 ◽

Author(s):

Stefani Giacopazzi ◽

Daniel Vong ◽

Alice Devigne ◽

Needhi Bhalla

Keyword(s):

Meiotic Prophase ◽

Spindle Checkpoint ◽

Specific Role ◽

Null Mutation ◽

Adapter Protein ◽

C Elegans ◽

Homolog Pairing ◽

Meiotic Chromosomes

AbstractThe conserved ATPase, PCH-2/TRIP13, is required during both the spindle checkpoint and meiotic prophase. However, it’s specific role in regulating meiotic homolog pairing, synapsis and recombination has been enigmatic. Here, we report that this enzyme is required to proofread meiotic homolog interactions. We generated a mutant version of PCH-2 in C. elegans that binds ATP but cannot hydrolyze it: pch-2E253Q. In vitro, this mutant binds its substrates but is unable to remodel them. This mutation results in non-homologous synapsis and loss of crossover assurance. Surprisingly, worms with a null mutation in PCH-2’s adapter protein, CMT-1, the ortholog of p31comet, localize PCH-2 to meiotic chromosomes, exhibit non-homologous synapsis and lose crossover assurance. The similarity in phenotypes between cmt-1 and pch-2E253Q mutants indicate that PCH-2 can bind its meiotic substrates in the absence of CMT-1, in contrast to its role during the spindle checkpoint, but requires its adapter to hydrolyze ATP and remodel them.

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The conserved AAA-ATPase PCH-2 TRIP13 regulates spindle checkpoint strength

Molecular Biology of the Cell ◽

10.1091/mbc.e20-05-0310 ◽

2020 ◽

Vol 31 (20) ◽

pp. 2219-2233

Author(s):

Lénaïg Défachelles ◽

Anna E. Russo ◽

Christian R. Nelson ◽

Needhi Bhalla

Keyword(s):

Cell Cycle ◽

Cell Volume ◽

Cell Fate ◽

Spindle Checkpoint ◽

Early Embryogenesis ◽

Aaa Atpase ◽

Cell Cycle Delay ◽

C Elegans

The length of the cell cycle delay imposed by the spindle checkpoint, also referred to as the spindle checkpoint strength, is controlled by the number of unattached kinetochores, cell volume, and cell fate. We show that PCH-2, a highly conserved AAA-ATPase, controls checkpoint strength during early embryogenesis in C. elegans.

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