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Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis†.

Publication ,  Journal Article
Li, S-Y; Gu, X; Heinrich, A; Hurley, EG; Capel, B; DeFalco, T
Published in: Biol Reprod
October 11, 2021

Testis differentiation is initiated when Sry in pre-Sertoli cells directs the gonad toward a male-specific fate. Sertoli cells are essential for testis development, but cell types within the interstitial compartment, such as immune and endothelial cells, are also critical for organ formation. Our previous work implicated macrophages in fetal testis morphogenesis, but little is known about genes underlying immune cell development during organogenesis. Here, we examine the role of the immune-associated genes Mafb and Maf in mouse fetal gonad development, and we demonstrate that deletion of these genes leads to aberrant hematopoiesis manifested by supernumerary gonadal monocytes. Mafb; Maf double knockout embryos underwent initial gonadal sex determination normally, but exhibited testicular hypervascularization, testis cord formation defects, Leydig cell deficit, and a reduced number of germ cells. In general, Mafb and Maf alone were dispensable for gonad development; however, when both genes were deleted, we observed significant defects in testicular morphogenesis, indicating that Mafb and Maf work redundantly during testis differentiation. These results demonstrate previously unappreciated roles for Mafb and Maf in immune and vascular development and highlight the importance of interstitial cells in gonadal differentiation.

Duke Scholars

Published In

Biol Reprod

DOI

EISSN

1529-7268

Publication Date

October 11, 2021

Volume

105

Issue

4

Start / End Page

958 / 975

Location

United States

Related Subject Headings

  • Testis
  • Proto-Oncogene Proteins c-maf
  • Organogenesis
  • Obstetrics & Reproductive Medicine
  • Myeloid Cells
  • Mice
  • Male
  • MafB Transcription Factor
  • Embryo, Mammalian
  • Animals
 

Citation

APA
Chicago
ICMJE
MLA
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Li, S.-Y., Gu, X., Heinrich, A., Hurley, E. G., Capel, B., & DeFalco, T. (2021). Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis†. Biol Reprod, 105(4), 958–975. https://doi.org/10.1093/biolre/ioab098
Li, Shu-Yun, Xiaowei Gu, Anna Heinrich, Emily G. Hurley, Blanche Capel, and Tony DeFalco. “Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis†.Biol Reprod 105, no. 4 (October 11, 2021): 958–75. https://doi.org/10.1093/biolre/ioab098.
Li S-Y, Gu X, Heinrich A, Hurley EG, Capel B, DeFalco T. Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis†. Biol Reprod. 2021 Oct 11;105(4):958–75.
Li, Shu-Yun, et al. “Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis†.Biol Reprod, vol. 105, no. 4, Oct. 2021, pp. 958–75. Pubmed, doi:10.1093/biolre/ioab098.
Li S-Y, Gu X, Heinrich A, Hurley EG, Capel B, DeFalco T. Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis†. Biol Reprod. 2021 Oct 11;105(4):958–975.
Journal cover image

Published In

Biol Reprod

DOI

EISSN

1529-7268

Publication Date

October 11, 2021

Volume

105

Issue

4

Start / End Page

958 / 975

Location

United States

Related Subject Headings

  • Testis
  • Proto-Oncogene Proteins c-maf
  • Organogenesis
  • Obstetrics & Reproductive Medicine
  • Myeloid Cells
  • Mice
  • Male
  • MafB Transcription Factor
  • Embryo, Mammalian
  • Animals