HSF-1-mediated cytoskeletal integrity determines thermotolerance and life span

被引：135

作者：

Baird, Nathan A. ^{[1
]}

Douglas, Peter M. ^{[1
]}

Simic, Milos S. ^{[1
]}

Grant, Ana R. ^{[2
]}

Moresco, James J. ^{[3
]}

Wolff, Suzanne C. ^{[1
]}

Yates, John R., III ^{[3
]}

Manning, Gerard ^{[4
]}

Dillin, Andrew ^{[1
]}

机构：

[1] Univ Calif Berkeley, Howard Hughes Med Inst, Berkeley, CA 94720 USA

[2] Univ Michigan, Sch Med, Dept Computat Med & Bioinformat, Ann Arbor, MI 48109 USA

[3] Scripps Res Inst, La Jolla, CA 92037 USA

[4] Genentech Inc, San Francisco, CA 94080 USA

来源：

SCIENCE | 2014年 / 346卷 / 6207期

关键词：

HEAT-SHOCK FACTOR-1; CAENORHABDITIS-ELEGANS; C.-ELEGANS; PROTEINS; TROPONIN; HSF1; ORGANIZATION; CONTRACTION; ENDOCYTOSIS; EXPRESSION;

D O I：

10.1126/science.1253168

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];

摘要：

The conserved heat shock transcription factor-1 (HSF-1) is essential to cellular stress resistance and life-span determination. The canonical function of HSF-1 is to regulate a network of genes encoding molecular chaperones that protect proteins from damage caused by extrinsic environmental stress or intrinsic age-related deterioration. In Caenorhabditis elegans, we engineered a modified HSF-1 strain that increased stress resistance and longevity without enhanced chaperone induction. This health assurance acted through the regulation of the calcium-binding protein PAT-10. Loss of pat-10 caused a collapse of the actin cytoskeleton, stress resistance, and life span. Furthermore, overexpression of pat-10 increased actin filament stability, thermotolerance, and longevity, indicating that in addition to chaperone regulation, HSF-1 has a prominent role in cytoskeletal integrity, ensuring cellular function during stress and aging.

引用

页码：360 / 363

页数：4

共 22 条

[1]

Genome-wide analysis identifies a general requirement for polarity proteins in endocytic traffic [J].

Balklava, Zita ;

Pant, Saumya ;

Fares, Hanna ;

Grant, Barth D. .

NATURE CELL BIOLOGY, 2007, 9 (09) :1066-U35

[2]

CYTOCHALASIN-D INHIBITS ACTIN POLYMERIZATION AND INDUCES DEPOLYMERIZATION OF ACTIN-FILAMENTS FORMED DURING PLATELET SHAPE CHANGE [J].

CASELLA, JF ;

FLANAGAN, MD ;

LIN, S .

NATURE, 1981, 293 (5830) :302-305

[3]

Heat shock proteins and heat shock factor 1 in carcinogenesis and tumor development: an update [J].

Ciocca, Daniel R. ;

Arrigo, Andre Patrick ;

Calderwood, Stuart K. .

ARCHIVES OF TOXICOLOGY, 2013, 87 (01) :19-48

[4]

Regulation of endocytosis by CUP-5, the Caenorhabditis elegans mucolipin-1 homolog [J].

Fares, H ;

Greenwald, I .

NATURE GENETICS, 2001, 28 (01) :64-68

[5]

Active HSF1 significantly suppresses polyglutamine aggregate formation in cellular and mouse models [J].

Fujimoto, M ;

Takaki, E ;

Hayashi, T ;

Kitaura, Y ;

Tanaka, Y ;

Inouye, S ;

Nakai, A .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (41) :34908-34916

[6]

Actin Dynamics Regulate Multiple Endosomal Steps during Kaposi's Sarcoma-Associated Herpesvirus Entry and Trafficking in Endothelial Cells [J].

Greene, Whitney ;

Gao, Shou-Jiang .

PLOS PATHOGENS, 2009, 5 (07)

[7]

The L-type cyclin CYL-1 and the heat-shock-factor HSF-1 are required for heat-shock-induced protein expression in Caenorhabditis elegans [J].

Hajdu-Cronin, YM ;

Chen, WJ ;

Sternberg, PW .

GENETICS, 2004, 168 (04) :1937-1949

[8]

Stochastic and genetic factors influence tissue-specific decline in ageing C-elegans [J].

Herndon, LA ;

Schmeissner, PJ ;

Dudaronek, JM ;

Brown, PA ;

Listner, KM ;

Sakano, Y ;

Paupard, MC ;

Hall, DH ;

Driscoll, M .

NATURE, 2002, 419 (6909) :808-814

[9]

Regulation of aging and age-related disease by DAF-16 and heat-shock factor [J].

Hsu, AL ;

Murphy, CT ;

Kenyon, C .

SCIENCE, 2003, 300 (5622) :1142-1145

[10]

Small heat-shock proteins protect from heat-stroke-associated neurodegeneration [J].

Kourtis, Nikos ;

Nikoletopoulou, Vassiliki ;

Tavernarakis, Nektarios .

NATURE, 2012, 490 (7419) :213-+

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