Oncotarget

Priority Research Papers:

Mitochondrial retrograde signaling inhibits the survival during prolong S/G2 arrest in Saccharomyces cerevisiae

Anna N. Zyrina, Maksim I. Sorokin, Sviatoslav S. Sokolov, Dmitry A. Knorre and Fedor F. Severin _

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Oncotarget. 2015; 6:44084-44094. https://doi.org/10.18632/oncotarget.6406

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Abstract

Anna N. Zyrina1,*, Maksim I. Sorokin2,*, Sviatoslav S. Sokolov2, Dmitry A. Knorre2, Fedor F. Severin2

1Faculty of Bioengineering and Bioinformatics, Moscow State University, Moscow, Russia

2Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow, Russia

*These authors contributed equally to this work

Correspondence to:

Fedor Severin, e-mail: severin@belozersky.msu.ru

Keywords: cell cycle arrest, telomere dysfunction, retrograde signaling, Rtg pathway, mitochondria

Received: September 30, 2015     Accepted: November 05, 2015     Published: November 27, 2015

ABSTRACT

Cell senescence is dependent on the arrest in cell cycle. Here we studied the role of mitochondrial retrograde response signaling in yeast cell survival under a prolonged arrest. We have found that, unlike G1, long-term arrest in mitosis or S phase results in a loss of colony-forming abilities. Consistent with previous observations, loss of mitochondrial DNA significantly increased the survival of arrested cells. We found that this was because the loss increases the duration of G1 phase. Unexpectedly, retrograde signaling, which is typically triggered by a variety of mitochondrial dysfunctions, was found to be a negative regulator of the survival after the release from S-phase arrest induced by the telomere replication defect. Deletion of retrograde response genes decreased the arrest-induced death in such cells, whereas deletion of negative regulator of retrograde signaling MKS1 had the opposite effect. We provide evidence that these effects are due to alleviation of the strength of the S-phase arrest.


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