Altered primordial germ cell migration in the absence of transforming growth factor beta signaling via ALK5

Susana M Chuva de Sousa Lopes, Sander van den Driesche, Rita L C Carvalho, Jonas Larsson, Bart Eggen, M Azim Surani, Christine L Mummery

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Transforming growth factor beta (TGFbeta) inhibits proliferation and promotes the migration of primordial germ cells (PGCs) towards explants of gonadal ridges in vitro. However, its effects in vivo are still unclear. Here, we analyzed the behavior of PGCs in embryos lacking TGFbeta signaling via the type I receptor ALK5. TGFbeta in vivo was neither a chemoattractant for PGCs, nor did it affect their proliferation during migration towards the gonadal ridges up to embryonic day (E)10. Unexpectedly, the absence of TGFbeta signaling in fact resulted in significant facilitation of PGC migration out of the hindgut, due to the reduced deposition of collagen type I surrounding the gut of Alk5-deficient mutant embryos. Migratory PGCs adhere strongly to collagen; therefore, reduced collagen type I along the gut may result in reduced adhesion, facilitating migration into the dorsal mesenterium and gonadal ridges. Our results provide new evidence for the role of TGFbeta signaling in migration of PGCs in vivo distinct from that described previously.

Original languageEnglish
Pages (from-to)194-203
Number of pages10
JournalDevelopmental Biology
Volume284
Issue number1
DOIs
Publication statusPublished - 1 Aug 2005

Keywords / Materials (for Non-textual outputs)

  • Activin Receptors, Type I
  • Animals
  • Blotting, Western
  • Cell Adhesion
  • Cell Movement
  • Collagen Type I
  • DNA Primers
  • Embryonic Development
  • Fluorescent Antibody Technique
  • Germ Cells
  • Immunohistochemistry
  • Mice
  • Protein-Serine-Threonine Kinases
  • Receptors, Transforming Growth Factor beta
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Transforming Growth Factor beta

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