title: Disruption of genital ridge development causes aberrant primordial germ cell proliferation but does not affect their directional migration.
abstract: BACKGROUND
  The directional migration and the following development of primordial germ cells (PGCs) during gonad formation are key steps for germline development. It has been proposed that the interaction between germ cells and genital ridge (GR) somatic cells plays essential roles in this process. However, the in vivo functional requirements of GR somatic cells in germ cell development are largely unknown.
  
  
  RESULTS
  Wt1 mutation (Wt1(R394W/R394W)) results in GR agenesis through mitotic arrest of coelomic epitheliums. In this study, we employed the GR-deficient mouse model, Wt1(R394W/R394W), to investigate the roles of GR somatic cells in PGC migration and proliferation. We found that the number of PGCs was dramatically reduced in GR-deficient embryos at embryonic day (E) 11.5 and E12.5 due to decreased proliferation of PGCs, involving low levels of BMP signaling. In contrast, the germ cells in Wt1(R394W/R394W) embryos were still mitotically active at E13.5, while all the germ cells in control embryos underwent mitotic arrest at this stage. Strikingly, the directional migration of PGCs was not affected by the absence of GR somatic cells. Most of the PGCs reached the mesenchyme under the coelomic epithelium at E10.5 and no ectopic PGCs were noted in GR-deficient embryos. However, the precise positioning of PGCs was disrupted.
  
  
  CONCLUSIONS
  Our work provides in vivo evidence that the proliferation of germ cells is precisely regulated by GR somatic cells during different stages of gonad development. GR somatic cells are probably dispensable for the directional migration of PGCs, but they are required for precise positioning of PGCs at the final step of migration.
authors.affiliation: State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, 1 Beichen West Road, Chaoyang District, Beijing, 100101, China.
authors.forename: Su-Ren
authors.initials: SR
authors.lastname: Chen
authors.forename: Qiao-Song
authors.initials: QS
authors.lastname: Zheng
authors.forename: Yang
authors.initials: Y
authors.lastname: Zhang
authors.forename: Fei
authors.initials: F
authors.lastname: Gao
authors.forename: Yi-Xun
authors.initials: YX
authors.lastname: Liu
mesh_terms: D000818:Animals; D002450:Cell Communication; D002452:Cell Count; D002465:Cell Movement; D049109:Cell Proliferation; D054377:Chemokine CXCL12 / Q000378:metabolism; D004622:Embryo, Mammalian / Q000166:cytology / Q000378:metabolism; D004848:Epithelium / Q000196:embryology / Q000378:metabolism; D005260:Female; D005854:Germ Cells / Q000166:cytology*; D006066:Gonads / Q000166:cytology* / Q000196:embryology*; D019012:Integrin beta1 / Q000378:metabolism; D008297:Male; D051379:Mice; D008938:Mitosis; D009154:Mutation / Q000235:genetics; D019849:Sex Determination Processes; D019089:Stem Cell Factor / Q000378:metabolism; D025721:WT1 Proteins / Q000235:genetics
chemical_list: D054377:Chemokine CXCL12; D019012:Integrin beta1; D019089:Stem Cell Factor; D025721:WT1 Proteins