RNA-seq of zebrafish embryos to investigate how Rbm8a deficiency akin to TAR Syndrome causes hematopoietic defects by modulating Wnt/PCP signaling

ABSTRACT: Defects in blood development are a major contributor to complex congenital anomalies. Thrombocytopenia-Absent Radius (TAR) Syndrome is a rare congenital disease presenting with reduced blood platelets (megakaryocytic thrombocytopenia) and forelimb anomalies, concurrent with variable heart and kidney defects caused by hypomorphic RBM8A/Y14 gene function. RBM8A encodes a component of the ubiquitous exon junction complex involved in mRNA splicing, transport, and nonsense-mediated decay. How perturbing a general mRNA-processing factor causes the distinct phenotypes of TAR Syndrome remains unknown. Here, we connect zebrafish rbm8a perturbation to early hematopoiesis defects via attenuated planar cell polarity (PCP) signaling involved in controlling developmental cell arrangements. Combining dif

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Danio rerio

SUBMITTER: Mark Robinson 

PROVIDER: E-MTAB-12503 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress