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            <title xml:lang="en">Hog1 and the homeostasis of telomeres during replicative senescence in saccharomyces cerevisiae</title>
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                <forename type="first">Bechara</forename>
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                <title xml:lang="en">Hog1 and the homeostasis of telomeres during replicative senescence in saccharomyces cerevisiae</title>
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                    <forename type="first">Maria Teresa</forename>
                    <surname>Teixeira</surname>
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                  <title>TELOMERES &amp; TELOMERASE</title>
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              <p>Telomeres protect linear chromosomes from fusions and degradations. However, the protective functions of telomeres are put at risk when they shorten as the cell divides without telomerase. When telomeres reach a critically short length, they trigger a DNA damage checkpoint-dependent cell cycle arrest in a process called replicative senescence. Data obtained in different organisms show that mitochondrial defects and oxidative stress accelerate telomere shortening and dysfunction. However, how ROS levels are produced and controlled during senescence is still elusive. In Saccharomyces cerevisiae, Hog1, the orthologue of p38 MAPK, is a major factor protecting against osmotic stress and regulating ROS levels. Hog1 activates the transcription of detoxifying genes but also interferes with mitochondrial functions and increases the levels of ROS. Here we show that in telomerase-negative cultures, ROS levels increase before senescence crisis, coinciding with the activation of Hog1. Deletion of Hog1 accelerates senescence demonstrating its contribution to cell viability in the absence of telomerase. Adding antioxidants delays senescence and partially suppresses the acceleration of senescence in hog1-delta cells, suggesting a role of Hog1 in regulating ROS levels during this process. ROS levels also increase during senescence when Mec1, the major DNA damage checkpoint in budding yeast, is mutated. However, Mec1 and Hog1 act on ROS through two independent signaling pathways that cooperate to keep ROS in check during senescence.</p>
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