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Article: A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

TitleA Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages
Authors
KeywordsBAMs
fate-mapping
macrophages ontogeny
microglia
SMAD4
Issue Date2023
Citation
Immunity, 2023, v. 56, n. 5, p. 1027-1045.e8 How to Cite?
AbstractGenetic tools to target microglia specifically and efficiently from the early stages of embryonic development are lacking. We generated a constitutive Cre line controlled by the microglia signature gene Crybb1 that produced nearly complete recombination in embryonic brain macrophages (microglia and border-associated macrophages [BAMs]) by the perinatal period, with limited recombination in peripheral myeloid cells. Using this tool in combination with Flt3-Cre lineage tracer, single-cell RNA-sequencing analysis, and confocal imaging, we resolved embryonic-derived versus monocyte-derived BAMs in the mouse cortex. Deletion of the transcription factor SMAD4 in microglia and embryonic-derived BAMs using Crybb1-Cre caused a developmental arrest of microglia, which instead acquired a BAM specification signature. By contrast, the development of genuine BAMs remained unaffected. Our results reveal that SMAD4 drives a transcriptional and epigenetic program that is indispensable for the commitment of brain macrophages to the microglia fate and highlight Crybb1-Cre as a tool for targeting embryonic brain macrophages.
Persistent Identifierhttp://hdl.handle.net/10722/334907
ISSN
2023 Impact Factor: 25.5
2023 SCImago Journal Rankings: 13.578
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBrioschi, Simone-
dc.contributor.authorBelk, Julia A.-
dc.contributor.authorPeng, Vincent-
dc.contributor.authorMolgora, Martina-
dc.contributor.authorRodrigues, Patrick Fernandes-
dc.contributor.authorNguyen, Khai M.-
dc.contributor.authorWang, Shoutang-
dc.contributor.authorDu, Siling-
dc.contributor.authorWang, Wei Le-
dc.contributor.authorGrajales-Reyes, Gary E.-
dc.contributor.authorPonce, Jennifer M.-
dc.contributor.authorYuede, Carla M.-
dc.contributor.authorLi, Qingyun-
dc.contributor.authorBaer, John M.-
dc.contributor.authorDeNardo, David G.-
dc.contributor.authorGilfillan, Susan-
dc.contributor.authorCella, Marina-
dc.contributor.authorSatpathy, Ansuman T.-
dc.contributor.authorColonna, Marco-
dc.date.accessioned2023-10-20T06:51:38Z-
dc.date.available2023-10-20T06:51:38Z-
dc.date.issued2023-
dc.identifier.citationImmunity, 2023, v. 56, n. 5, p. 1027-1045.e8-
dc.identifier.issn1074-7613-
dc.identifier.urihttp://hdl.handle.net/10722/334907-
dc.description.abstractGenetic tools to target microglia specifically and efficiently from the early stages of embryonic development are lacking. We generated a constitutive Cre line controlled by the microglia signature gene Crybb1 that produced nearly complete recombination in embryonic brain macrophages (microglia and border-associated macrophages [BAMs]) by the perinatal period, with limited recombination in peripheral myeloid cells. Using this tool in combination with Flt3-Cre lineage tracer, single-cell RNA-sequencing analysis, and confocal imaging, we resolved embryonic-derived versus monocyte-derived BAMs in the mouse cortex. Deletion of the transcription factor SMAD4 in microglia and embryonic-derived BAMs using Crybb1-Cre caused a developmental arrest of microglia, which instead acquired a BAM specification signature. By contrast, the development of genuine BAMs remained unaffected. Our results reveal that SMAD4 drives a transcriptional and epigenetic program that is indispensable for the commitment of brain macrophages to the microglia fate and highlight Crybb1-Cre as a tool for targeting embryonic brain macrophages.-
dc.languageeng-
dc.relation.ispartofImmunity-
dc.subjectBAMs-
dc.subjectfate-mapping-
dc.subjectmacrophages ontogeny-
dc.subjectmicroglia-
dc.subjectSMAD4-
dc.titleA Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.immuni.2023.01.028-
dc.identifier.pmid36791722-
dc.identifier.scopuseid_2-s2.0-85149918726-
dc.identifier.volume56-
dc.identifier.issue5-
dc.identifier.spage1027-
dc.identifier.epage1045.e8-
dc.identifier.eissn1097-4180-
dc.identifier.isiWOS:001005029200001-

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