DC Element | Wert | Sprache |
dc.contributor.author | Ivy, Jessica R. | |
dc.contributor.author | Drechsler, Maik | |
dc.contributor.author | Catterson, James H. | |
dc.contributor.author | Bodmer, Rolf | |
dc.contributor.author | Ocorr, Karen | |
dc.contributor.author | Paululat, Achim | |
dc.contributor.author | Hartley, Paul S. | |
dc.date.accessioned | 2021-12-23T16:19:09Z | - |
dc.date.available | 2021-12-23T16:19:09Z | - |
dc.date.issued | 2015 | |
dc.identifier.issn | 19326203 | |
dc.identifier.uri | https://osnascholar.ub.uni-osnabrueck.de/handle/unios/13008 | - |
dc.description.abstract | Insect nephrocytes are highly endocytic scavenger cells that represent the only invertebrate model for the study of human kidney podocytes. Despite their importance, nephrocyte development is largely uncharacterised. This work tested whether the insect ortholog of mammalian Kidney Kruppel-Like Factor (Klf15), a transcription factor required for mammalian podocyte differentiation, was required for insect nephrocyte development. It was found that expression of Drosophila Klf15 (dKlf15, previously known as Bteb2) was restricted to the only two nephrocyte populations in Drosophila, the garland cells and pericardial nephrocytes. Loss of dKlf15 function led to attrition of both nephrocyte populations and sensitised larvae to the xenotoxin silver nitrate. Although pericardial nephrocytes in dKlf15 loss of function mutants were specified during embryogenesis, they failed to express the slit diaphragm gene sticks and stones and did not form slit diaphragms. Conditional silencing of dKlf15 in adults led to reduced surface expression of the endocytic receptor Amnionless and loss of in vivo scavenger function. Over-expression of dKlf15 increased nephrocyte numbers and rescued age-dependent decline in nephrocyte function. The data place dKlf15 upstream of sns and Amnionless in a nephrocyte-restricted differentiation pathway and suggest dKlf15 expression is both necessary and sufficient to sustain nephrocyte differentiation. These findings explain the physiological relevance of dKlf15 in Drosophila and imply that the role of KLF15 in human podocytes is evolutionarily conserved. | |
dc.description.sponsorship | British Heart Foundation Intermediate Basic Science Fellowship [FS/13/17/29905]; British Heart Foundation Centre of Research Excellence (CoRE) award; Scottish Universities Life Science Alliance (SULSA); American Heart AssociationAmerican Heart Association [0835243N]; AHAAmerican Heart Association [14GRNT20490239]; NIHUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [R01 HL054732, P01 HL098053, P01 AG033561]; DFGGerman Research Foundation (DFG)European Commission [SFB944]; DAAD/IPID program; British Heart FoundationBritish Heart Foundation [FS/13/17/29905] Funding Source: researchfish; NATIONAL HEART, LUNG, AND BLOOD INSTITUTEUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Heart Lung & Blood Institute (NHLBI) [R01HL054732, P01HL098053] Funding Source: NIH RePORTER; NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of General Medical Sciences (NIGMS) [R01GM084947] Funding Source: NIH RePORTER; NATIONAL INSTITUTE ON AGINGUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute on Aging (NIA) [P01AG033561] Funding Source: NIH RePORTER; PSH is supported by a British Heart Foundation Intermediate Basic Science Fellowship (FS/13/17/29905). This work was also supported by a British Heart Foundation Centre of Research Excellence (CoRE) award to the University of Edinburgh and by a subsistence grant from the Scottish Universities Life Science Alliance (SULSA) to PSH. KO is supported by American Heart Association award 0835243N. KO is supported by AHA grant 14GRNT20490239. RB is supported by NIH grants R01 HL054732, P01 HL098053, P01 AG033561. A.P. received support from the DFG (SFB944) and the DAAD/IPID program. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. | |
dc.language.iso | en | |
dc.publisher | PUBLIC LIBRARY SCIENCE | |
dc.relation.ispartof | PLOS ONE | |
dc.subject | CARDIAC-FUNCTION | |
dc.subject | CUBILIN | |
dc.subject | DYNAMICS | |
dc.subject | ENHANCER | |
dc.subject | GENE-EXPRESSION | |
dc.subject | HEART | |
dc.subject | INSECT | |
dc.subject | Multidisciplinary Sciences | |
dc.subject | PERICARDIAL CELLS | |
dc.subject | REGULATOR | |
dc.subject | Science & Technology - Other Topics | |
dc.subject | ULTRASTRUCTURE | |
dc.title | Klf15 Is Critical for the Development and Differentiation of Drosophila Nephrocytes | |
dc.type | journal article | |
dc.identifier.doi | 10.1371/journal.pone.0134620 | |
dc.identifier.isi | ISI:000359951900007 | |
dc.description.volume | 10 | |
dc.description.issue | 8 | |
dc.contributor.orcid | 0000-0003-2782-0490 | |
dc.contributor.orcid | 0000-0003-1004-4376 | |
dc.contributor.orcid | 0000-0002-8845-6859 | |
dc.contributor.orcid | 0000-0003-4231-0114 | |
dc.contributor.researcherid | AAY-6150-2021 | |
dc.publisher.place | 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA | |
dcterms.isPartOf.abbreviation | PLoS One | |
dcterms.oaStatus | gold, Green Accepted, Green Published | |
crisitem.author.dept | FB 05 - Biologie/Chemie | - |
crisitem.author.deptid | fb05 | - |
crisitem.author.orcid | 0000-0002-8845-6859 | - |
crisitem.author.parentorg | Universität Osnabrück | - |
crisitem.author.netid | PaAc947 | - |