The effect of neuronal expression of heat shock proteins 26 and 27 on lifespan, neurodegeneration, and apoptosis in Drosophila

doi:10.1016/j.bbrc.2008.08.161

Biochemical and Biophysical Research Communications

Volume 376, Issue 4, 28 November 2008, Pages 637-641

https://doi.org/10.1016/j.bbrc.2008.08.161 Get rights and content

Abstract

Heat shock proteins (Hsps) are chaperones thought to increase lifespan, enhance stress resistance, and prevent apoptosis and neurodegenerative diseases. Our previous study reported that ubiquitous expression of hsp26 or hsp27 extended Drosophila lifespan. The effect of neuronal expression of hsp26 and hsp27 in Drosophila on the above-mentioned functions has not yet been investigated. Here, we show that neuronal expression of hsp26 or hsp27 improved lifespan and increased resistance to oxidative stress. However, only neuronal expression of hsp27 ameliorated Parkinsonism climbing disorder and attenuated mild polyglutamine-induced toxicity. Additionally, neuronal expression of hsp27 specifically partially rescued hid-induced lethality, but was not able to rescue reaper/grim-induced lethality. However, unlike hsp27, neuronal expression of hsp26 did not rescue hid-induced or reaper/grim-induced lethality. In summary, we demonstrate the functional similarities and differences of neuronal expression of hsp26 and hsp27 in adult Drosophila.

Section snippets

Materials and methods

Fly strains. UAS-hsp26 and UAS-hsp27 have been described previously [9]. UAS-reaper, UAS-hid, and UAS-grim were obtained from Dr. Ann-Shyn Chiang’s lab. Double UAS lines, UAS-rpr;UAS-hsp26, UAS-rpr;UAS-hsp27, UAS-hid;UAS-hsp26, UAS-hid;UAS-hsp27, UAS-grim;UAS-hsp26, and UAS-grim; UAS-hsp27 were generated. A pan-neuronal driver, elav-GAL4, was used to induce transgene expression. GMR-GAL4/Cyo;UAS-41Q and GMR-GAL4/Cyo;UAS-127Q were obtained from Dr. Seymour Benzer’s lab. All flies were raised on

Neuronal overexpression of hsp26 or hsp27 increases lifespan and resistance to oxidative stress in Drosophila

Our previous study showed that ubiquitous expression of hsp26 or hsp27 increases Drosophila lifespan and resistance to oxidative stress [9]. Neuronal tissue is suggested to be important for the control of lifespan [14]. To examine whether neuronal overexpression of hsp26 or hsp27 is sufficient to extend lifespan, we measured the lifespan of flies overexpressing hsp26 or hsp27 by the elav-GAL4, and of the corresponding control flies, at 25 °C. There is an increase of approximately 32–44% in the

Acknowledgments

This study was supported by grants from the National Science Council (NSC-96-2311-B-007-003) and the APEX from the Brain Research Center at National Tsing-Hua University to H.-D. Wang.

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¹: These authors contributed equally to this work.

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The effect of neuronal expression of heat shock proteins 26 and 27 on lifespan, neurodegeneration, and apoptosis in Drosophila

Abstract

Section snippets

Materials and methods

Neuronal overexpression of hsp26 or hsp27 increases lifespan and resistance to oxidative stress in Drosophila

Acknowledgments

Exp. Gerontol.

Mech. Ageing Dev.

J. Biol. Chem.

J. Biol. Chem.

J. Biol. Chem.

Neurotoxicology

Mol. Ther.

Cell

J. Biol. Chem.

Molecular chaperones in the cytosol: from nascent chain to folded protein

Science

Posttranslational quality control: folding, refolding, and degrading proteins

Science

Molecular chaperones—cellular machines for protein folding

Angew. Chem. Int. Ed. Engl.

Regulation of heat shock gene induction and expression during Drosophila development

Cell. Mol. Life Sci.

Drosophila as a model for human neurodegenerative disease

Annu. Rev. Genet.

Heat shock genes—integrating cell survival and death

J. Biosci.

Chaperoning extended life

Nature

Multiple-stress analysis for isolation of Drosophila longevity genes

Proc. Natl. Acad. Sci. USA

Overexpression of the small mitochondrial Hsp22 extends Drosophila life span and increases resistance to oxidative stress

FASEB J.

Regulation of aging and age-related disease by DAF-16 and heat-shock factor

Science

Lifespan extension in C. elegans by a molecular chaperone dependent upon insulin-like signals

Aging Cell

Regulation of longevity in Caenorhabditis elegans by heat shock factor and molecular chaperones

Mol. Biol. Cell