APC/CCDH1 synchronizes ribose-5-phosphate levels and DNA synthesis to cell cycle progression
Identifieur interne : 000B26 ( Main/Merge ); précédent : 000B25; suivant : 000B27APC/CCDH1 synchronizes ribose-5-phosphate levels and DNA synthesis to cell cycle progression
Auteurs : Yang Li [République populaire de Chine] ; Cui-Fang Yao [République populaire de Chine] ; Fu-Jiang Xu [République populaire de Chine] ; Yuan-Yuan Qu [République populaire de Chine] ; Jia-Tao Li [République populaire de Chine] ; Yan Lin [République populaire de Chine] ; Zhong-Lian Cao [République populaire de Chine] ; Peng-Cheng Lin [République populaire de Chine] ; Wei Xu [République populaire de Chine] ; Shi-Min Zhao [République populaire de Chine] ; Jian-Yuan Zhao [République populaire de Chine]Source :
- Nature Communications [ 2041-1723 ] ; 2019.
Abstract
Accumulation of nucleotide building blocks prior to and during S phase facilitates DNA duplication. Herein, we find that the anaphase-promoting complex/cyclosome (APC/C) synchronizes ribose-5-phosphate levels and DNA synthesis during the cell cycle. In late G1 and S phases, transketolase-like 1 (TKTL1) is overexpressed and forms stable TKTL1-transketolase heterodimers that accumulate ribose-5-phosphate. This accumulation occurs by asymmetric production of ribose-5-phosphate from the non-oxidative pentose phosphate pathway and prevention of ribose-5-phosphate removal by depleting transketolase homodimers. In the G2 and M phases after DNA synthesis, expression of the APC/C adaptor CDH1 allows APC/CCDH1 to degrade D-box-containing TKTL1, abrogating ribose-5-phosphate accumulation by TKTL1. TKTL1-overexpressing cancer cells exhibit elevated ribose-5-phosphate levels. The low CDH1 or high TKTL1-induced accumulation of ribose-5-phosphate facilitates nucleotide and DNA synthesis as well as cell cycle progression in a ribose-5-phosphate-saturable manner. Here we reveal that the cell cycle control machinery regulates DNA synthesis by mediating ribose-5-phosphate sufficiency.
Url:
DOI: 10.1038/s41467-019-10375-x
PubMed: 31175280
PubMed Central: 6555833
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PMC:6555833Le document en format XML
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synchronizes ribose-5-phosphate levels and DNA synthesis to cell cycle progression</title>
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<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
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</author>
<author><name sortKey="Cao, Zhong Lian" sort="Cao, Zhong Lian" uniqKey="Cao Z" first="Zhong-Lian" last="Cao">Zhong-Lian Cao</name>
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<institution>School of Pharmacy,</institution>
<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Lin, Peng Cheng" sort="Lin, Peng Cheng" uniqKey="Lin P" first="Peng-Cheng" last="Lin">Peng-Cheng Lin</name>
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<institution>Key Laboratory for Tibet Plateau Phytochemistry of Qinghai Province, College of Pharmacy,</institution>
<institution>Qinghai University for Nationalities,</institution>
</institution-wrap>
Xining, 810007 P. R. China</nlm:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Xining</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Xu, Wei" sort="Xu, Wei" uniqKey="Xu W" first="Wei" last="Xu">Wei Xu</name>
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<institution-id institution-id-type="GRID">grid.8547.e</institution-id>
<institution>Obstetrics & Gynecology Hospital of Fudan University, State Key Laboratory of Genetic Engineering, School of Life Sciences and Institutes of Biomedical Sciences,</institution>
<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
</affiliation>
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<institution-id institution-id-type="GRID">grid.8547.e</institution-id>
<institution>Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,</institution>
<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0807 1581</institution-id>
<institution-id institution-id-type="GRID">grid.13291.38</institution-id>
<institution>Collaborative Innovation Center for Biotherapy, West China Hospital,</institution>
<institution>Sichuan University,</institution>
</institution-wrap>
Chengdu, 610041 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Chengdu</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Zhao, Shi Min" sort="Zhao, Shi Min" uniqKey="Zhao S" first="Shi-Min" last="Zhao">Shi-Min Zhao</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0125 2443</institution-id>
<institution-id institution-id-type="GRID">grid.8547.e</institution-id>
<institution>Obstetrics & Gynecology Hospital of Fudan University, State Key Laboratory of Genetic Engineering, School of Life Sciences and Institutes of Biomedical Sciences,</institution>
<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0125 2443</institution-id>
<institution-id institution-id-type="GRID">grid.8547.e</institution-id>
<institution>Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,</institution>
<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0807 1581</institution-id>
<institution-id institution-id-type="GRID">grid.13291.38</institution-id>
<institution>Collaborative Innovation Center for Biotherapy, West China Hospital,</institution>
<institution>Sichuan University,</institution>
</institution-wrap>
Chengdu, 610041 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Chengdu</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Zhao, Jian Yuan" sort="Zhao, Jian Yuan" uniqKey="Zhao J" first="Jian-Yuan" last="Zhao">Jian-Yuan Zhao</name>
<affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0125 2443</institution-id>
<institution-id institution-id-type="GRID">grid.8547.e</institution-id>
<institution>Obstetrics & Gynecology Hospital of Fudan University, State Key Laboratory of Genetic Engineering, School of Life Sciences and Institutes of Biomedical Sciences,</institution>
<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0125 2443</institution-id>
<institution-id institution-id-type="GRID">grid.8547.e</institution-id>
<institution>Key Laboratory of Reproduction Regulation of NPFPC and Collaborative Innovation Center for Genetics and Development, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases,</institution>
<institution>Fudan University,</institution>
</institution-wrap>
Shanghai, 200438 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Shanghai</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="Aff6"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0807 1581</institution-id>
<institution-id institution-id-type="GRID">grid.13291.38</institution-id>
<institution>Collaborative Innovation Center for Biotherapy, West China Hospital,</institution>
<institution>Sichuan University,</institution>
</institution-wrap>
Chengdu, 610041 P.R. China</nlm:aff>
<country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country>
<wicri:regionArea>Chengdu</wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Nature Communications</title>
<idno type="eISSN">2041-1723</idno>
<imprint><date when="2019">2019</date>
</imprint>
</series>
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<front><div type="abstract" xml:lang="en"><p id="Par1">Accumulation of nucleotide building blocks prior to and during S phase facilitates DNA duplication. Herein, we find that the anaphase-promoting complex/cyclosome (APC/C) synchronizes ribose-5-phosphate levels and DNA synthesis during the cell cycle. In late G<sub>1</sub>
and S phases, transketolase-like 1 (TKTL1) is overexpressed and forms stable TKTL1-transketolase heterodimers that accumulate ribose-5-phosphate. This accumulation occurs by asymmetric production of ribose-5-phosphate from the non-oxidative pentose phosphate pathway and prevention of ribose-5-phosphate removal by depleting transketolase homodimers. In the G<sub>2</sub>
and M phases after DNA synthesis, expression of the APC/C adaptor CDH1 allows APC/C<sup>CDH1</sup>
to degrade D-box-containing TKTL1, abrogating ribose-5-phosphate accumulation by TKTL1. TKTL1-overexpressing cancer cells exhibit elevated ribose-5-phosphate levels. The low CDH1 or high TKTL1-induced accumulation of ribose-5-phosphate facilitates nucleotide and DNA synthesis as well as cell cycle progression in a ribose-5-phosphate-saturable manner. Here we reveal that the cell cycle control machinery regulates DNA synthesis by mediating ribose-5-phosphate sufficiency.</p>
</div>
</front>
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<author><name sortKey="Krause, Kh" uniqKey="Krause K">KH Krause</name>
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<biblStruct><analytic><author><name sortKey="Xu, Xj" uniqKey="Xu X">XJ Xu</name>
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<author><name sortKey="Zur Hausen, A" uniqKey="Zur Hausen A">A zur Hausen</name>
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<author><name sortKey="Coy, Jf" uniqKey="Coy J">JF Coy</name>
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<author><name sortKey="Lochelt, M" uniqKey="Lochelt M">M Lochelt</name>
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