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GAS1 Deficient Enhances UPR Activity in Saccharomyces cerevisiae.


ABSTRACT: Beta-1,3-glucanosyltransferase (Gas1p) plays important roles in cell wall biosynthesis and morphogenesis and has been implicated in DNA damage responses and cell cycle regulation in fungi. Yeast Gas1p has also been reported to participate in endoplasmic reticulum (ER) stress responses. However, the precise roles and molecular mechanisms through which Gas1p affects these responses have yet to be elucidated. In this study, we constructed GAS1-deficient (gas1?) and GAS1-overexpressing (GAS1 OE) yeast strains and observed that the gas1? strain exhibited a decreased proliferation ability and a shorter replicative lifespan (RLS), as well as enhanced activity of the unfolded protein response (UPR) in the absence of stress. However, under the high-tunicamycin-concentration (an ER stress-inducing agent; 1.0??g/mL) stress, the gas1? yeast cells exhibited an increased proliferation ability compared with the wild-type yeast strain. In addition, our findings demonstrated that IRE1 and HAC1 (two upstream modulators of the UPR) are required for the survival of gas1? yeast cells under the tunicamycin stress. On the other hand, we provided evidence that the GAS1 overexpression caused an obvious sensitivity to the low-tunicamycin-concentration (0.25??g/mL). Collectively, our results indicate that Gas1p plays an important role in the ageing and ER stress responses in yeast.

SUBMITTER: Cui HJ 

PROVIDER: S-EPMC6582843 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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<i>GAS1</i> Deficient Enhances UPR Activity in <i>Saccharomyces cerevisiae</i>.

Cui Hong-Jing HJ   Cui Xin-Gang XG   Jing Xia X   Yuan Yuan Y   Chen Ya-Qin YQ   Sun Ya-Xin YX   Zhao Wei W   Liu Xin-Guang XG  

BioMed research international 20190602


Beta-1,3-glucanosyltransferase (Gas1p) plays important roles in cell wall biosynthesis and morphogenesis and has been implicated in DNA damage responses and cell cycle regulation in fungi. Yeast Gas1p has also been reported to participate in endoplasmic reticulum (ER) stress responses. However, the precise roles and molecular mechanisms through which Gas1p affects these responses have yet to be elucidated. In this study, we constructed <i>GAS1-</i>deficient (<i>gas1Δ</i>) and <i>GAS1</i>-overexp  ...[more]

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