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Lack of Gata3 results in conotruncal heart anomalies in mouse

机译：缺乏Gata3会导致小鼠圆锥锥性心脏异常

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The transcription factor Gata3 is an important regulator of the development of thymus, the nervous system, ear, kidney, and adrenal glands. This study analyzes the role of Gata3 in the developing heart using a mouse strain containing an nlsLacZ reporter gene fused in frame to the Gata3 gene by homologous recombination. Using in situ hybridization, RT-PCR and Gata3-LacZ histochemistry, Gata3 expression was shown in various cardiac structures up to newborn stage. During looping stages (E9.5-E11.5) Gata3-LacZ activity recapitulated endogenous Gata3 and was abundantly expressed in the endocardial ridges and endothelium of distal outflow tract. Strong reporter gene expression was also noted in the mesenchyme of ventral branchial arches, and in the epithelium. In the atrioventricular canal expression was relatively lower. In the four-chambered heart stages (E13.5-E17.5) the LacZ-staining did not recapitulate the endogenous Gata3 transcript and showed rather lineage tracing of formerly Gata3-expressing cells in the hearts. beta-Galactosidase activity was detected in the cusps of semilunar valves, aorta, pulmonary trunk, innominate and common carotid arteries, and faintly in the atrioventricular valves. Gata3-null embryos die normally between E11 and E12. Pharmacological treatment with sympathomimetic beta-adrenergic receptor agonist lengthens the survival up to E18 when malformations of the heart such as ventricular septal defect (VSD), double-outlet of right ventricle (DORV), anomalies of the aortic arch (AAA) and persistent truncus arteriosus (PTA) were detected. The specified malformations correlate with the normal developmental pattern of Gata3-LacZ expression. The short outflow tract and insufficient rotation of truncus arteriosus during looping stages might be the main reasons underlying these malformations.
机译：转录因子Gata3是胸腺，神经系统，耳朵，肾脏和肾上腺发育的重要调节剂。这项研究使用含有nlsLacZ报告基因的小鼠品系，通过同源重组与Gata3基因框内融合，分析了Gata3在发育中的心脏中的作用。使用原位杂交，RT-PCR和Gata3-LacZ组织化学，显示Gata3在直至新生阶段的各种心脏结构中表达。在循环阶段（E9.5-E11.5），Gata3-LacZ活性概括了内源性Gata3，并在远端流出道的心内膜和内皮中大量表达。在腹侧branch弓的间充质和上皮细胞中也发现了强大的报告基因表达。在房室管中的表达相对较低。在四腔心期（E13.5-E17.5）中，LacZ染色不能概括内源性Gata3转录本，而在心脏中显示的是以前表达Gata3的细胞的血统谱系。 β-半乳糖苷酶活性在半月瓣，主动脉，肺干，无名和颈总动脉的尖端以及房室瓣微弱。 Gata3无效的胚胎通常在E11和E12之间死亡。当心脏畸形，例如室间隔缺损（VSD），右心室双出口（DORV），主动脉弓畸形（AAA）和持续性截骨等心脏畸形时，用拟交感神经药β-肾上腺素能受体激动剂进行药理治疗可使生存期延长至E18。检测到动脉（PTA）。特定的畸形与Gata3-LacZ表达的正常发育模式相关。在循环阶段短动脉流出道和动脉干旋转不足可能是导致这些畸形的主要原因。

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