Developmental Dynamics · 2016 · 22 citations · 67 references
Life SciencesCell BiologyDevelopmental BiologyDevelopmental Cell BiologyEmbryologyGastrulationEmbryonic Germ LayersGerm Cell DevelopmentGerm Layer DifferentiationGerm Layer FormationGerm Layer PatterningPrimordial Germ Cell DevelopmentBlimp1-dependent Germ Cell SpecificationEpiblast DifferentiationGerm Cell Lineage SpecificationHindgut MorphologyMaternal-fetal Interface DevelopmentPosterior Epiblast PatterningPrimordial Germ Cell DifferentiationPrimordial Germ Cell Lineage Segregation
BACKGROUND: PRDM1 is a transcriptional repressor that contributes to primordial germ cell (PGC) development. During early gastrulation, epiblast-derived PRDM1 is thought to be restricted to a lineage-segregated germ line in the allantois. However, given recent findings that PGCs overlap an allantoic progenitor pool that contributes widely to the fetal-umbilical interface, posterior PRDM1 may also contribute to soma. RESULTS: Within the posterior mouse gastrula (early streak, 12-s stages, embryonic days ∼6.75-9.0), PRDM1 localized to all tissues containing putative PGCs; however, PRDM1 was also found in all three primary germ layers, their derivatives, and two presumptive growth centers, the allantoic core domain and ventral ectodermal ridge. While PRDM1 and STELLA colocalized predominantly within the hindgut, where putative PGCs reside, other colocalizing cells were found in non-PGC sites. Additional PRDM1 and STELLA cells were found independent of each other throughout the posterior region, including the hindgut. The Prdm1-Cre-driven reporter supported PRDM1 localization in the majority of sites; however, some Prdm1 descendants were found in sites independent of PRDM1 protein, including allantoic mesothelium and hindgut endoderm. CONCLUSIONS: Posterior PRDM1 contributes more broadly to the developing fetal-maternal connection than previously recognized, and PRDM1 and STELLA, while overlapping in putative PGCs, also co-localize in several other tissues. Developmental Dynamics 246:50-71, 2017. © 2016 Wiley Periodicals, Inc.
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