Deficiency of Caenorhabditis elegans RecQ5 homologue reduces life span and increases sensitivity to ionizing radiation

Yun Seong Jeong; Yool Le Kang; Ki Ho Lim; Myon Hee Lee; Jiyeung Lee; Hyeon Sook Koo

doi:10.1016/j.dnarep.2003.07.003

Deficiency of Caenorhabditis elegans RecQ5 homologue reduces life span and increases sensitivity to ionizing radiation

Yun Seong Jeong, Yool Le Kang, Ki Ho Lim, Myon Hee Lee, Jiyeung Lee, Hyeon Sook Koo

Department of Biochemistry

Research output: Contribution to journal › Article › peer-review

26 Citations (Scopus)

Abstract

Gene expression and RNA interference phenotypes were investigated for a Caenorhabditis elegans homologue (Ce-RCQ-5) of human RecQ5 protein. Expression of the mRNA was observed by in situ hybridization from earliest embryogenesis and gradually decreased during late embryogenesis. Ce-RCQ-5 was immuno-localized in the nuclei of embryos, germ cells, and oocytes and also in the nuclei of various somatic cells of larvae and adults. Despite ubiquitous expression in postembryonic cells, RCQ-5 protein expression was highest in intestinal cells, which was confirmed by tagging the gene expression with green fluorescence protein. When endogenous Ce-rcq-5 gene expression was inhibited by RNA interference, no clear phenotypes were observed during development. However, C. elegans life span was reduced by 37% due to RNA interference of rcq-5 gene, suggesting its possible role in maintenance of genomic stability, as has been ascribed to other RecQ family DNA helicases. In addition, C. elegans became significantly more sensitive to ionizing radiation after inhibition of rcq-5 gene expression, indicating an involvement of C. elegans RCQ-5 in a cellular response to DNA damage, possibly in DNA repair.

Original language	English
Pages (from-to)	1309-1319
Number of pages	11
Journal	DNA Repair
Volume	2
Issue number	12
DOIs	https://doi.org/10.1016/j.dnarep.2003.07.003
Publication status	Published - 2003 Dec 9

Bibliographical note

Funding Information:
We thank Dr. Alan Coulson (Sanger Center) for the E03A3 cosmid clone, Andrew Fire (Carnegie institute) for pPD95.75 vector, and Robert Barstead (Oklahoma Medical Research Foundation) for RB835 strain. N2, RB835, CB1597 C. elegans strains were obtained from C. elegans Genetics Center (St. Paul, MN), which is supported by the National Center for Research Resources. This work was supported by the Life Phenomena & Function Research Grant [01-J-LF-01-B-83] and Atomic Energy Basic Research Grant [98-f-12] from the Korean Ministry of Science and Technology to H.-S. Koo.

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.dnarep.2003.07.003

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title = "Deficiency of Caenorhabditis elegans RecQ5 homologue reduces life span and increases sensitivity to ionizing radiation",

abstract = "Gene expression and RNA interference phenotypes were investigated for a Caenorhabditis elegans homologue (Ce-RCQ-5) of human RecQ5 protein. Expression of the mRNA was observed by in situ hybridization from earliest embryogenesis and gradually decreased during late embryogenesis. Ce-RCQ-5 was immuno-localized in the nuclei of embryos, germ cells, and oocytes and also in the nuclei of various somatic cells of larvae and adults. Despite ubiquitous expression in postembryonic cells, RCQ-5 protein expression was highest in intestinal cells, which was confirmed by tagging the gene expression with green fluorescence protein. When endogenous Ce-rcq-5 gene expression was inhibited by RNA interference, no clear phenotypes were observed during development. However, C. elegans life span was reduced by 37% due to RNA interference of rcq-5 gene, suggesting its possible role in maintenance of genomic stability, as has been ascribed to other RecQ family DNA helicases. In addition, C. elegans became significantly more sensitive to ionizing radiation after inhibition of rcq-5 gene expression, indicating an involvement of C. elegans RCQ-5 in a cellular response to DNA damage, possibly in DNA repair.",

author = "Jeong, {Yun Seong} and Kang, {Yool Le} and Lim, {Ki Ho} and Lee, {Myon Hee} and Jiyeung Lee and Koo, {Hyeon Sook}",

note = "Funding Information: We thank Dr. Alan Coulson (Sanger Center) for the E03A3 cosmid clone, Andrew Fire (Carnegie institute) for pPD95.75 vector, and Robert Barstead (Oklahoma Medical Research Foundation) for RB835 strain. N2, RB835, CB1597 C. elegans strains were obtained from C. elegans Genetics Center (St. Paul, MN), which is supported by the National Center for Research Resources. This work was supported by the Life Phenomena & Function Research Grant [01-J-LF-01-B-83] and Atomic Energy Basic Research Grant [98-f-12] from the Korean Ministry of Science and Technology to H.-S. Koo. ",

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doi = "10.1016/j.dnarep.2003.07.003",

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T1 - Deficiency of Caenorhabditis elegans RecQ5 homologue reduces life span and increases sensitivity to ionizing radiation

AU - Jeong, Yun Seong

AU - Kang, Yool Le

AU - Lim, Ki Ho

AU - Lee, Myon Hee

AU - Lee, Jiyeung

AU - Koo, Hyeon Sook

N1 - Funding Information: We thank Dr. Alan Coulson (Sanger Center) for the E03A3 cosmid clone, Andrew Fire (Carnegie institute) for pPD95.75 vector, and Robert Barstead (Oklahoma Medical Research Foundation) for RB835 strain. N2, RB835, CB1597 C. elegans strains were obtained from C. elegans Genetics Center (St. Paul, MN), which is supported by the National Center for Research Resources. This work was supported by the Life Phenomena & Function Research Grant [01-J-LF-01-B-83] and Atomic Energy Basic Research Grant [98-f-12] from the Korean Ministry of Science and Technology to H.-S. Koo.

PY - 2003/12/9

Y1 - 2003/12/9

N2 - Gene expression and RNA interference phenotypes were investigated for a Caenorhabditis elegans homologue (Ce-RCQ-5) of human RecQ5 protein. Expression of the mRNA was observed by in situ hybridization from earliest embryogenesis and gradually decreased during late embryogenesis. Ce-RCQ-5 was immuno-localized in the nuclei of embryos, germ cells, and oocytes and also in the nuclei of various somatic cells of larvae and adults. Despite ubiquitous expression in postembryonic cells, RCQ-5 protein expression was highest in intestinal cells, which was confirmed by tagging the gene expression with green fluorescence protein. When endogenous Ce-rcq-5 gene expression was inhibited by RNA interference, no clear phenotypes were observed during development. However, C. elegans life span was reduced by 37% due to RNA interference of rcq-5 gene, suggesting its possible role in maintenance of genomic stability, as has been ascribed to other RecQ family DNA helicases. In addition, C. elegans became significantly more sensitive to ionizing radiation after inhibition of rcq-5 gene expression, indicating an involvement of C. elegans RCQ-5 in a cellular response to DNA damage, possibly in DNA repair.

AB - Gene expression and RNA interference phenotypes were investigated for a Caenorhabditis elegans homologue (Ce-RCQ-5) of human RecQ5 protein. Expression of the mRNA was observed by in situ hybridization from earliest embryogenesis and gradually decreased during late embryogenesis. Ce-RCQ-5 was immuno-localized in the nuclei of embryos, germ cells, and oocytes and also in the nuclei of various somatic cells of larvae and adults. Despite ubiquitous expression in postembryonic cells, RCQ-5 protein expression was highest in intestinal cells, which was confirmed by tagging the gene expression with green fluorescence protein. When endogenous Ce-rcq-5 gene expression was inhibited by RNA interference, no clear phenotypes were observed during development. However, C. elegans life span was reduced by 37% due to RNA interference of rcq-5 gene, suggesting its possible role in maintenance of genomic stability, as has been ascribed to other RecQ family DNA helicases. In addition, C. elegans became significantly more sensitive to ionizing radiation after inhibition of rcq-5 gene expression, indicating an involvement of C. elegans RCQ-5 in a cellular response to DNA damage, possibly in DNA repair.

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Deficiency of Caenorhabditis elegans RecQ5 homologue reduces life span and increases sensitivity to ionizing radiation

Abstract

Bibliographical note

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