BROWSE

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Rhee, Hyun-Woo
Biomimetic Chemistry Lab
Research Interests
  • Site-Specific Protein Labeling in Living Cells
  • Artificial Cofactors for Biomimetic Catalyst
  • Spatiotemporal Proteome mapping of living cells

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A metazoan ortholog of SpoT hydrolyzes ppGpp and functions in starvation responses

Cited 16 times inthomson ciCited 13 times inthomson ci
Title
A metazoan ortholog of SpoT hydrolyzes ppGpp and functions in starvation responses
Author
Sun, DaweiLee, GinaLee, Jun HeeKim, Hye-YeonRhee, Hyun-WooPark, Seung-YeolKim, Kyung-JinKim, YongsungKim, Bo YeonHong, Jong-InPark, ChankyuChoy, Hyon E.Kim, Jung HoeJeon, Young HoChung, Jongkyeong
Keywords
ESCHERICHIA-COLI; STRINGENT RESPONSE; STREPTOMYCES-ANTIBIOTICUS; GUANOSINE TETRAPHOSPHATE; PROTEIN-SYNTHESIS; (P)PPGPP; BACTERIAL; RELA; GENE; ACID
Issue Date
2010-10
Publisher
NATURE PUBLISHING GROUP
Citation
NATURE STRUCTURAL & MOLECULAR BIOLOGY, v.17, no.10, pp.1188 - +
Abstract
In nutrient-starved bacteria, RelA and SpoT proteins have key roles in reducing cell growth and overcoming stresses. Here we identify functional SpoT orthologs in metazoa (named Mesh1, encoded by HDDC3 in human and Q9VAM9 in Drosophila melanogaster) and reveal their structures and functions. Like the bacterial enzyme, Mesh1 proteins contain an active site for ppGpp hydrolysis and a conserved His-Asp-box motif for Mn 2+ binding. Consistent with these structural data, Mesh1 efficiently catalyzes hydrolysis of guanosine 3′,5′-diphosphate (ppGpp) both in vitro and in vivo. Mesh1 also suppresses SpoT-deficient lethality and RelA-induced delayed cell growth in bacteria. Notably, deletion of Mesh1 (Q9VAM9) in Drosophila induces retarded body growth and impaired starvation resistance. Microarray analyses reveal that the amino acid-starved Mesh1 null mutant has highly downregulated DNA and protein synthesis-related genes and upregulated stress-responsible genes. These data suggest that metazoan SpoT orthologs have an evolutionarily conserved function in starvation responses.
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DOI
10.1038/nsmb.1906
ISSN
1545-9993
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PHY_Journal Papers
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