Rgs6 is required for adult maintenance of dopaminergic neurons in the ventral substantia nigra.
Identifieur interne : 000622 ( PubMed/Corpus ); précédent : 000621; suivant : 000623Rgs6 is required for adult maintenance of dopaminergic neurons in the ventral substantia nigra.
Auteurs : Panojot Bifsha ; Jianqi Yang ; Rory A. Fisher ; Jacques DrouinSource :
- PLoS genetics [ 1553-7404 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Dopaminergic Neurons (physiology), Homeodomain Proteins (metabolism), Mice, Inbred C57BL, Mice, Knockout, Organ Specificity, Parkinson Disease (genetics), Parkinson Disease (pathology), RGS Proteins (physiology), Signal Transduction, Substantia Nigra (pathology), Transcription Factors (metabolism).
- MESH :
- chemical , metabolism : Homeodomain Proteins, Transcription Factors.
- genetics : Parkinson Disease.
- pathology : Parkinson Disease, Substantia Nigra.
- physiology : Dopaminergic Neurons, RGS Proteins.
- Animals, Mice, Inbred C57BL, Mice, Knockout, Organ Specificity, Signal Transduction.
Abstract
Parkinson disease (PD) is characterized by the preferential, but poorly understood, vulnerability to degeneration of midbrain dopaminergic (mDA) neurons in the ventral substantia nigra compacta (vSNc). These sensitive mDA neurons express Pitx3, a transcription factor that is critical for their survival during development. We used this dependence to identify, by flow cytometry and expression profiling, the negative regulator of G-protein signaling Rgs6 for its restricted expression in these neurons. In contrast to Pitx3-/- mDA neurons that die during fetal (vSNc) or post-natal (VTA) period, the vSNc mDA neurons of Rgs6-/- mutant mice begin to exhibit unilateral signs of degeneration at around 6 months of age, and by one year cell loss is observed in a fraction of mice. Unilateral cell loss is accompanied by contralateral degenerating neurons that exhibit smaller cell size, altered morphology and reduced dendritic network. The degenerating neurons have low levels of tyrosine hydroxylase (TH) and decreased nuclear Pitx3; accordingly, expression of many Pitx3 target gene products is altered, including Vmat2, Bdnf, Aldh1a1 (Adh2) and Fgf10. These low TH neurons also express markers of increased dopamine signaling, namely increased DAT and phospho-Erk1/2 expression. The late onset degeneration may reflect the protective action of Rgs6 against excessive DA signaling throughout life. Rgs6-dependent protection is thus critical for adult survival and maintenance of the vSNc mDA neurons that are most affected in PD.
DOI: 10.1371/journal.pgen.1004863
PubMed: 25501001
Links to Exploration step
pubmed:25501001Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Rgs6 is required for adult maintenance of dopaminergic neurons in the ventral substantia nigra.</title><author><name sortKey="Bifsha, Panojot" sort="Bifsha, Panojot" uniqKey="Bifsha P" first="Panojot" last="Bifsha">Panojot Bifsha</name><affiliation><nlm:affiliation>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec, Canada; Division of Experimental Medicine, McGill University, Montréal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jianqi" sort="Yang, Jianqi" uniqKey="Yang J" first="Jianqi" last="Yang">Jianqi Yang</name><affiliation><nlm:affiliation>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Fisher, Rory A" sort="Fisher, Rory A" uniqKey="Fisher R" first="Rory A" last="Fisher">Rory A. Fisher</name><affiliation><nlm:affiliation>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Drouin, Jacques" sort="Drouin, Jacques" uniqKey="Drouin J" first="Jacques" last="Drouin">Jacques Drouin</name><affiliation><nlm:affiliation>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec, Canada; Division of Experimental Medicine, McGill University, Montréal, Quebec, Canada.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25501001</idno><idno type="pmid">25501001</idno><idno type="doi">10.1371/journal.pgen.1004863</idno><idno type="wicri:Area/PubMed/Corpus">000622</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000622</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Rgs6 is required for adult maintenance of dopaminergic neurons in the ventral substantia nigra.</title><author><name sortKey="Bifsha, Panojot" sort="Bifsha, Panojot" uniqKey="Bifsha P" first="Panojot" last="Bifsha">Panojot Bifsha</name><affiliation><nlm:affiliation>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec, Canada; Division of Experimental Medicine, McGill University, Montréal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jianqi" sort="Yang, Jianqi" uniqKey="Yang J" first="Jianqi" last="Yang">Jianqi Yang</name><affiliation><nlm:affiliation>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Fisher, Rory A" sort="Fisher, Rory A" uniqKey="Fisher R" first="Rory A" last="Fisher">Rory A. Fisher</name><affiliation><nlm:affiliation>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Drouin, Jacques" sort="Drouin, Jacques" uniqKey="Drouin J" first="Jacques" last="Drouin">Jacques Drouin</name><affiliation><nlm:affiliation>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec, Canada; Division of Experimental Medicine, McGill University, Montréal, Quebec, Canada.</nlm:affiliation></affiliation></author></analytic><series><title level="j">PLoS genetics</title><idno type="eISSN">1553-7404</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Dopaminergic Neurons (physiology)</term><term>Homeodomain Proteins (metabolism)</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Organ Specificity</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>RGS Proteins (physiology)</term><term>Signal Transduction</term><term>Substantia Nigra (pathology)</term><term>Transcription Factors (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Homeodomain Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dopaminergic Neurons</term><term>RGS Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Organ Specificity</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson disease (PD) is characterized by the preferential, but poorly understood, vulnerability to degeneration of midbrain dopaminergic (mDA) neurons in the ventral substantia nigra compacta (vSNc). These sensitive mDA neurons express Pitx3, a transcription factor that is critical for their survival during development. We used this dependence to identify, by flow cytometry and expression profiling, the negative regulator of G-protein signaling Rgs6 for its restricted expression in these neurons. In contrast to Pitx3-/- mDA neurons that die during fetal (vSNc) or post-natal (VTA) period, the vSNc mDA neurons of Rgs6-/- mutant mice begin to exhibit unilateral signs of degeneration at around 6 months of age, and by one year cell loss is observed in a fraction of mice. Unilateral cell loss is accompanied by contralateral degenerating neurons that exhibit smaller cell size, altered morphology and reduced dendritic network. The degenerating neurons have low levels of tyrosine hydroxylase (TH) and decreased nuclear Pitx3; accordingly, expression of many Pitx3 target gene products is altered, including Vmat2, Bdnf, Aldh1a1 (Adh2) and Fgf10. These low TH neurons also express markers of increased dopamine signaling, namely increased DAT and phospho-Erk1/2 expression. The late onset degeneration may reflect the protective action of Rgs6 against excessive DA signaling throughout life. Rgs6-dependent protection is thus critical for adult survival and maintenance of the vSNc mDA neurons that are most affected in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25501001</PMID><DateCreated><Year>2014</Year><Month>12</Month><Day>16</Day></DateCreated><DateCompleted><Year>2015</Year><Month>11</Month><Day>06</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7404</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>12</Issue><PubDate><Year>2014</Year><Month>Dec</Month></PubDate></JournalIssue><Title>PLoS genetics</Title><ISOAbbreviation>PLoS Genet.</ISOAbbreviation></Journal><ArticleTitle>Rgs6 is required for adult maintenance of dopaminergic neurons in the ventral substantia nigra.</ArticleTitle><Pagination><MedlinePgn>e1004863</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pgen.1004863</ELocationID><Abstract><AbstractText>Parkinson disease (PD) is characterized by the preferential, but poorly understood, vulnerability to degeneration of midbrain dopaminergic (mDA) neurons in the ventral substantia nigra compacta (vSNc). These sensitive mDA neurons express Pitx3, a transcription factor that is critical for their survival during development. We used this dependence to identify, by flow cytometry and expression profiling, the negative regulator of G-protein signaling Rgs6 for its restricted expression in these neurons. In contrast to Pitx3-/- mDA neurons that die during fetal (vSNc) or post-natal (VTA) period, the vSNc mDA neurons of Rgs6-/- mutant mice begin to exhibit unilateral signs of degeneration at around 6 months of age, and by one year cell loss is observed in a fraction of mice. Unilateral cell loss is accompanied by contralateral degenerating neurons that exhibit smaller cell size, altered morphology and reduced dendritic network. The degenerating neurons have low levels of tyrosine hydroxylase (TH) and decreased nuclear Pitx3; accordingly, expression of many Pitx3 target gene products is altered, including Vmat2, Bdnf, Aldh1a1 (Adh2) and Fgf10. These low TH neurons also express markers of increased dopamine signaling, namely increased DAT and phospho-Erk1/2 expression. The late onset degeneration may reflect the protective action of Rgs6 against excessive DA signaling throughout life. Rgs6-dependent protection is thus critical for adult survival and maintenance of the vSNc mDA neurons that are most affected in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bifsha</LastName><ForeName>Panojot</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec, Canada; Division of Experimental Medicine, McGill University, Montréal, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Jianqi</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fisher</LastName><ForeName>Rory A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Drouin</LastName><ForeName>Jacques</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec, Canada; Division of Experimental Medicine, McGill University, Montréal, Quebec, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA161882</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA161882</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>MOP-123213</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal 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Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C433629">homeobox protein PITX3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Development. 2009 Feb;136(4):531-40</RefSource><PMID Version="1">19144721</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2011 Jan 14;286(2):1409-19</RefSource><PMID Version="1">21041304</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res Mol Brain Res. 2003 Jun 10;114(2):123-31</RefSource><PMID Version="1">12829322</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2010 Nov 26;107(11):1345-9</RefSource><PMID Version="1">20864673</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2014 Jul;124(7):3032-46</RefSource><PMID Version="1">24865427</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1999 Oct 15;19(20):8839-48</RefSource><PMID Version="1">10516303</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2011 Sep 7;31(36):12802-15</RefSource><PMID Version="1">21900559</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2005 Jul 1;14(13):1709-25</RefSource><PMID Version="1">15888489</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Neurobiol. 2011 Sep 1;94(4):389-407</RefSource><PMID Version="1">21723913</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res Gene Expr Patterns. 2002 Oct;1(3-4):199-203</RefSource><PMID Version="1">12638132</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2010 Dec;13(12):1481-8</RefSource><PMID Version="1">21057506</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuron. 2010 Jun 10;66(5):646-61</RefSource><PMID Version="1">20547124</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Histochem Cytochem. 2009 Dec 29;42(6):171-9</RefSource><PMID Version="1">20126570</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Parkinsons Dis. 2011;1(3):229-51</RefSource><PMID Version="1">23939304</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2014 Apr;28(4):1735-44</RefSource><PMID Version="1">24421401</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2001 Apr;77(2):558-67</RefSource><PMID Version="1">11299318</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2004 Sep 21;101(38):13891-6</RefSource><PMID Version="1">15353588</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2012 Feb 10;287(7):4972-81</RefSource><PMID Version="1">22179605</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4245-50</RefSource><PMID Version="1">12655058</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Pharmacol Sci. 2013 Sep;34(9):489-96</RefSource><PMID Version="1">23968642</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Struct Funct. 2012 Apr;217(2):591-612</RefSource><PMID Version="1">21935672</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Neurobiol. 2010 Feb 9;90(2):146-56</RefSource><PMID Version="1">19925845</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Dev Biol. 2007 Jul 15;307(2):421-33</RefSource><PMID Version="1">17540357</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Biochem Biophys. 2009;54(1-3):33-46</RefSource><PMID Version="1">19521673</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2008 Jul;11(7):755-61</RefSource><PMID Version="1">18536709</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2006 Jan;96(1):160-70</RefSource><PMID Version="1">16269007</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2005 Feb;18(1):19-31</RefSource><PMID Version="1">15649693</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Development. 2011 Dec;138(23):5213-22</RefSource><PMID Version="1">22069189</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2007 Jul 25;27(30):8138-48</RefSource><PMID Version="1">17652604</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2006 Aug;98(3):951-61</RefSource><PMID Version="1">16771836</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2012 Jan;27(1):8-30</RefSource><PMID Version="1">22081500</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2012 Sep 25;109(39):15918-23</RefSource><PMID Version="1">23019375</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1997 Feb 1;17(3):960-74</RefSource><PMID Version="1">8994051</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2009 Jul;12(7):826-8</RefSource><PMID Version="1">19503083</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Development. 2007 Jul;134(14):2673-84</RefSource><PMID Version="1">17592014</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2014 Oct;70:190-203</RefSource><PMID Version="1">24969022</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2009 Nov 20;465(3):214-9</RefSource><PMID Version="1">19766170</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2007 May 30;1150:55-61</RefSource><PMID Version="1">17397812</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Development. 2003 Jun;130(11):2535-42</RefSource><PMID Version="1">12702666</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Med. 2010 Jun;16(6):653-61</RefSource><PMID Version="1">20495568</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Pharmacol. 2007 May;71(5):1222-32</RefSource><PMID Version="1">17267664</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2010 Nov 26;107(11):1350-4</RefSource><PMID Version="1">20884879</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2013 Jun;125(6):932-43</RefSource><PMID Version="1">23331067</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2002 Jul 19;277(29):26200-7</RefSource><PMID Version="1">12011080</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Neurobiol. 2011 Apr;43(2):107-13</RefSource><PMID Version="1">21086067</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Front Neuroanat. 2010 Oct 20;4:140</RefSource><PMID Version="1">21079748</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2005 Feb 23;25(8):2132-7</RefSource><PMID Version="1">15728853</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2009 Dec;36(3):494-508</RefSource><PMID Version="1">19766189</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Aging. 2009 May;30(5):731-8</RefSource><PMID Version="1">17905480</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2001 May 22;98(11):6423-8</RefSource><PMID Version="1">11353855</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Neurobiol. 2006 Jan;78(1):1-16</RefSource><PMID Version="1">16414173</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Aging Cell. 2003 Apr;2(2):105-10</RefSource><PMID Version="1">12882323</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059290" MajorTopicYN="N">Dopaminergic Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018398" MajorTopicYN="N">Homeodomain Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" 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