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RNA-seq data analysis of Smad5 knockout and wild type individual mouse amnion samples collected during early embryonic development

ABSTRACT: Mice deficient in the BMP-effector, Smad5 (Smad5 KO), develop severe defects in embryonic morphogenesis as well as a delay in amnion-chorion separation, important extraembryonic tissues. After closure of the proamniotic canal, a remarkable ectopic primitive streak-like aggregate develops in the amnion of these mutants. We investigated the earliest steps of mutant amnion misdifferentiation by RNAseq of single Control (Ctrl) and Smad5 KO amnion samples collected before the appearance of the aggregate. The transcriptome analysis revealed two separate sets of non-squamous amnion defects. One set of mutants (KO-SetA) robustly overexpressed streak mesoderm-related genes conform former analyses (Pereira et al., 2012). The other set overexpressed extraembryonic ectoderm markers suggestive of chorionic inclusion in amnion (KO-SetB). Tetraploid chimera analyses confirmed that SMAD5 deficiency in the epiblast can result in two distinct sets of amnion defects: one with impaired anterior amnion expansion and differentiation, and another with inclusion of chorionic extraembryonic ectoderm in the space normally occupied by amnion.

ORGANISM(S): Mus musculus

PROVIDER: GSE99211 | GEO | 2018/06/15

REPOSITORIES: GEO

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