RNA interference against the putative insulin receptor substrate gene chico affects metamorphosis in Leptinotarsa decemlineata.
Identifieur interne : 000513 ( Main/Exploration ); précédent : 000512; suivant : 000514RNA interference against the putative insulin receptor substrate gene chico affects metamorphosis in Leptinotarsa decemlineata.
Auteurs : Pan Deng [République populaire de Chine] ; Qing-Yu Xu [République populaire de Chine] ; Kai-Yun Fu [République populaire de Chine] ; Wen-Chao Guo [République populaire de Chine] ; Guo-Qing Li [République populaire de Chine]Source :
- Insect biochemistry and molecular biology [ 1879-0240 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Coléoptères (croissance et développement), Coléoptères (génétique), Coléoptères (métabolisme), Ecdystérone (génétique), Hormones juvéniles (génétique), Interférence par ARN (MeSH), Larve (croissance et développement), Larve (génétique), Métamorphose biologique (génétique), Phosphatidylinositol 3-kinase (génétique), Protéines d'insecte (génétique), Récepteur à l'insuline (génétique).
- MESH :
- croissance et développement : Coléoptères, Larve.
- génétique : Coléoptères, Ecdystérone, Hormones juvéniles, Larve, Métamorphose biologique, Phosphatidylinositol 3-kinase, Protéines d'insecte, Récepteur à l'insuline.
- métabolisme : Coléoptères.
- Animaux, Interférence par ARN.
English descriptors
- KwdEn :
- Animals (MeSH), Coleoptera (genetics), Coleoptera (growth & development), Coleoptera (metabolism), Ecdysterone (genetics), Insect Proteins (genetics), Juvenile Hormones (genetics), Larva (genetics), Larva (growth & development), Metamorphosis, Biological (genetics), Phosphatidylinositol 3-Kinase (genetics), RNA Interference (MeSH), Receptor, Insulin (genetics).
- MESH :
- chemical , genetics : Ecdysterone, Insect Proteins, Juvenile Hormones, Phosphatidylinositol 3-Kinase, Receptor, Insulin.
- genetics : Coleoptera, Larva, Metamorphosis, Biological.
- growth & development : Coleoptera, Larva.
- metabolism : Coleoptera.
- Animals, RNA Interference.
Abstract
It is noted that insect insulin/insulin-like growth factor/target of rapamycin signaling is critical for the regulation of metamorphosis in holometabolous insects. However, the molecular mechanism remains undetermined. Our previous findings reveal that RNA interference (RNAi)-mediated knockdown of an insulin gene (LdILP2) in Leptinotarsa decemlineata disturbs both 20-hydroxyecdysone (20E) and juvenile hormone (JH) signaling, and impairs pupation. In the present paper, we further observed that the expression of the insulin receptor substrate gene chico (Ldchico) and the phosphoinositide-3-kinase gene pi3k (Ldpi3k92E) was repressed in LdILP2 depleted larvae. Moreover, RNAi of Ldchico or Ldpi3k92E decreased food consumption, affected absorption and metabolism of amino acids and sugars, and reduced expression of several 20E (LdEcR, LdHR3 and LdE75) and JH (LdJHAMT, LdKr-h1 and LdHairy) signaling genes. As a result, larval development was postponed and larval growth was inhibited. Intriguingly, knockdown of Ldchico, rather than Ldpi3k92E, impaired larval-pupal and pupal-adult ecdysis, and specifically repressed transcription of another 20E signaling gene LdUSP. Ingestion of 20E rescued the expression of LdEcR, LdHR3 and LdE75, whereas 20E feeding restored neither the decreased LdUSP mRNA level, nor the reduced pupation and adult emergence rates in Ldchico RNAi larvae. Therefore, Chico is critical for the regulation of larval-pupal-adult transition by a PI3K-independent pathway, perhaps through activation of USP in L. decemlineata.
DOI: 10.1016/j.ibmb.2018.10.001
PubMed: 30296480
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Electronic address: 197268973@qq.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095</wicri:regionArea><wicri:noRegion>210095</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Qing Yu" sort="Xu, Qing Yu" uniqKey="Xu Q" first="Qing-Yu" last="Xu">Qing-Yu Xu</name><affiliation wicri:level="1"><nlm:affiliation>Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095, China. Electronic address: xuqingyu21@126.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095</wicri:regionArea><wicri:noRegion>210095</wicri:noRegion></affiliation></author><author><name sortKey="Fu, Kai Yun" sort="Fu, Kai Yun" uniqKey="Fu K" first="Kai-Yun" last="Fu">Kai-Yun Fu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Plant Protection, Xinjiang Academy of Agricultural Sciences, Urumqi, 830091, China. 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Electronic address: ligq@njau.edu.cn.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095</wicri:regionArea><wicri:noRegion>210095</wicri:noRegion></affiliation></author></analytic><series><title level="j">Insect biochemistry and molecular biology</title><idno type="eISSN">1879-0240</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Coleoptera (genetics)</term><term>Coleoptera (growth & development)</term><term>Coleoptera (metabolism)</term><term>Ecdysterone (genetics)</term><term>Insect Proteins (genetics)</term><term>Juvenile Hormones (genetics)</term><term>Larva (genetics)</term><term>Larva (growth & development)</term><term>Metamorphosis, Biological (genetics)</term><term>Phosphatidylinositol 3-Kinase (genetics)</term><term>RNA Interference (MeSH)</term><term>Receptor, Insulin (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Coléoptères (croissance et développement)</term><term>Coléoptères (génétique)</term><term>Coléoptères (métabolisme)</term><term>Ecdystérone (génétique)</term><term>Hormones juvéniles (génétique)</term><term>Interférence par ARN (MeSH)</term><term>Larve (croissance et développement)</term><term>Larve (génétique)</term><term>Métamorphose biologique (génétique)</term><term>Phosphatidylinositol 3-kinase (génétique)</term><term>Protéines d'insecte (génétique)</term><term>Récepteur à l'insuline (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ecdysterone</term><term>Insect Proteins</term><term>Juvenile Hormones</term><term>Phosphatidylinositol 3-Kinase</term><term>Receptor, Insulin</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Coléoptères</term><term>Larve</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coleoptera</term><term>Larva</term><term>Metamorphosis, Biological</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Coleoptera</term><term>Larva</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Coléoptères</term><term>Ecdystérone</term><term>Hormones juvéniles</term><term>Larve</term><term>Métamorphose biologique</term><term>Phosphatidylinositol 3-kinase</term><term>Protéines d'insecte</term><term>Récepteur à l'insuline</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Coleoptera</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Coléoptères</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>RNA Interference</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Interférence par ARN</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It is noted that insect insulin/insulin-like growth factor/target of rapamycin signaling is critical for the regulation of metamorphosis in holometabolous insects. However, the molecular mechanism remains undetermined. Our previous findings reveal that RNA interference (RNAi)-mediated knockdown of an insulin gene (LdILP2) in Leptinotarsa decemlineata disturbs both 20-hydroxyecdysone (20E) and juvenile hormone (JH) signaling, and impairs pupation. In the present paper, we further observed that the expression of the insulin receptor substrate gene chico (Ldchico) and the phosphoinositide-3-kinase gene pi3k (Ldpi3k92E) was repressed in LdILP2 depleted larvae. Moreover, RNAi of Ldchico or Ldpi3k92E decreased food consumption, affected absorption and metabolism of amino acids and sugars, and reduced expression of several 20E (LdEcR, LdHR3 and LdE75) and JH (LdJHAMT, LdKr-h1 and LdHairy) signaling genes. As a result, larval development was postponed and larval growth was inhibited. Intriguingly, knockdown of Ldchico, rather than Ldpi3k92E, impaired larval-pupal and pupal-adult ecdysis, and specifically repressed transcription of another 20E signaling gene LdUSP. Ingestion of 20E rescued the expression of LdEcR, LdHR3 and LdE75, whereas 20E feeding restored neither the decreased LdUSP mRNA level, nor the reduced pupation and adult emergence rates in Ldchico RNAi larvae. Therefore, Chico is critical for the regulation of larval-pupal-adult transition by a PI3K-independent pathway, perhaps through activation of USP in L. decemlineata.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30296480</PMID><DateCompleted><Year>2019</Year><Month>05</Month><Day>21</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0240</ISSN><JournalIssue CitedMedium="Internet"><Volume>103</Volume><PubDate><Year>2018</Year><Month>12</Month></PubDate></JournalIssue><Title>Insect biochemistry and molecular biology</Title><ISOAbbreviation>Insect Biochem Mol Biol</ISOAbbreviation></Journal><ArticleTitle>RNA interference against the putative insulin receptor substrate gene chico affects metamorphosis in Leptinotarsa decemlineata.</ArticleTitle><Pagination><MedlinePgn>1-11</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0965-1748(18)30298-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ibmb.2018.10.001</ELocationID><Abstract><AbstractText>It is noted that insect insulin/insulin-like growth factor/target of rapamycin signaling is critical for the regulation of metamorphosis in holometabolous insects. However, the molecular mechanism remains undetermined. Our previous findings reveal that RNA interference (RNAi)-mediated knockdown of an insulin gene (LdILP2) in Leptinotarsa decemlineata disturbs both 20-hydroxyecdysone (20E) and juvenile hormone (JH) signaling, and impairs pupation. In the present paper, we further observed that the expression of the insulin receptor substrate gene chico (Ldchico) and the phosphoinositide-3-kinase gene pi3k (Ldpi3k92E) was repressed in LdILP2 depleted larvae. Moreover, RNAi of Ldchico or Ldpi3k92E decreased food consumption, affected absorption and metabolism of amino acids and sugars, and reduced expression of several 20E (LdEcR, LdHR3 and LdE75) and JH (LdJHAMT, LdKr-h1 and LdHairy) signaling genes. As a result, larval development was postponed and larval growth was inhibited. Intriguingly, knockdown of Ldchico, rather than Ldpi3k92E, impaired larval-pupal and pupal-adult ecdysis, and specifically repressed transcription of another 20E signaling gene LdUSP. Ingestion of 20E rescued the expression of LdEcR, LdHR3 and LdE75, whereas 20E feeding restored neither the decreased LdUSP mRNA level, nor the reduced pupation and adult emergence rates in Ldchico RNAi larvae. Therefore, Chico is critical for the regulation of larval-pupal-adult transition by a PI3K-independent pathway, perhaps through activation of USP in L. decemlineata.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Pan</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095, China. Electronic address: 197268973@qq.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Qing-Yu</ForeName><Initials>QY</Initials><AffiliationInfo><Affiliation>Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095, China. Electronic address: xuqingyu21@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fu</LastName><ForeName>Kai-Yun</ForeName><Initials>KY</Initials><AffiliationInfo><Affiliation>Department of Plant Protection, Xinjiang Academy of Agricultural Sciences, Urumqi, 830091, China. Electronic address: fukaiyun000@foxmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guo</LastName><ForeName>Wen-Chao</ForeName><Initials>WC</Initials><AffiliationInfo><Affiliation>Department of Plant Protection, Xinjiang Academy of Agricultural Sciences, Urumqi, 830091, China; Xinjiang Laboratory of Special Environmental Microbiology, Institute of Microbiology, Xinjiang Academy of Agricultural Sciences, Urumqi, 830091, China. Electronic address: gwc1966@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Guo-Qing</ForeName><Initials>GQ</Initials><AffiliationInfo><Affiliation>Education Ministry Key Laboratory of Integrated Management of Crop Diseases and Pests, College of Plant Protection, Nanjing Agricultural University, Nanjing, 210095, China. Electronic address: ligq@njau.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>10</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Insect Biochem Mol Biol</MedlineTA><NlmUniqueID>9207282</NlmUniqueID><ISSNLinking>0965-1748</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019476">Insect Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007605">Juvenile Hormones</NameOfSubstance></Chemical><Chemical><RegistryNumber>5289-74-7</RegistryNumber><NameOfSubstance UI="D004441">Ecdysterone</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.137</RegistryNumber><NameOfSubstance UI="D058539">Phosphatidylinositol 3-Kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D011972">Receptor, Insulin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001517" MajorTopicYN="N">Coleoptera</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004441" MajorTopicYN="N">Ecdysterone</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019476" MajorTopicYN="N">Insect Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007605" MajorTopicYN="N">Juvenile Hormones</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007814" MajorTopicYN="N">Larva</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008675" MajorTopicYN="N">Metamorphosis, Biological</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058539" MajorTopicYN="N">Phosphatidylinositol 3-Kinase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011972" MajorTopicYN="N">Receptor, Insulin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Adult emergence</Keyword><Keyword MajorTopicYN="Y">Insulin receptor substrate</Keyword><Keyword MajorTopicYN="Y">Leptinotarsa decemlineata</Keyword><Keyword MajorTopicYN="Y">Pupation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>08</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>09</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>10</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>10</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>5</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>10</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30296480</ArticleId><ArticleId IdType="pii">S0965-1748(18)30298-4</ArticleId><ArticleId IdType="doi">10.1016/j.ibmb.2018.10.001</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Deng, Pan" sort="Deng, Pan" uniqKey="Deng P" first="Pan" last="Deng">Pan Deng</name></noRegion><name sortKey="Fu, Kai Yun" sort="Fu, Kai Yun" uniqKey="Fu K" first="Kai-Yun" last="Fu">Kai-Yun Fu</name><name sortKey="Guo, Wen Chao" sort="Guo, Wen Chao" uniqKey="Guo W" first="Wen-Chao" last="Guo">Wen-Chao Guo</name><name sortKey="Li, Guo Qing" sort="Li, Guo Qing" uniqKey="Li G" first="Guo-Qing" last="Li">Guo-Qing Li</name><name sortKey="Xu, Qing Yu" sort="Xu, Qing Yu" uniqKey="Xu Q" first="Qing-Yu" last="Xu">Qing-Yu Xu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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