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Tbx1 is necessary for palatal elongation and elevation

机译：Tbx1对于pa骨的伸长和升高是必需的

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The transcription factor TBX1 is a key mediator of developmental abnormalities associated with DiGeorge/Velocardiofacial Syndrome Studies in mice have demonstrated that decreased dosage of Tbx1 results in defects in pharyngeal arch, cardiovascular, and craniofacial development The role of Tbx1 in cardiac development has been intensely studied, however, its role in palatal development is poorly understood By studying the Tbx1-/- mice we found defects during the critical points of palate elongation and elevation. The intrinsic palate defects in the Tbx1-/- mice we're determined by measuring changes in palate shelf length, proliferation, apoptosis, expression of relevant growth factors, and in palate fusion assays. Tbx1-/- embryos exhibit cleft palate with failed palate elevation in 100% and abnormal palatal-oral fusions in 50% In the Tbx1-/- mice the palate shelf length was reduced and tongue height was greater, demonstrating a physical impediment to palate elevation and apposition. In vitro palate fusion assays demonstrate that Tbx1-/- palate shelves are capable of fusion but a roller culture assay showed that the null palatal shelves were unable to elongate Diminished hyaluronic acid production in the Tbx1-/- palate shelves may explain failed palate shelf elevation In addition, cell proliferation and apoptosis were perturbed in Tbx1-/- palates A sharp decrease of Fgf8 expression was detected in the Tbx1-/- palate shelves, suggesting that Fgf8 is dependent on Tbx1 in the palate Fgf10 is also up-regulated in the Tbx1-/- palate shelves and tongue These data demonstrate that Tbx1 is a critical transcription factor that guides palatal elongation and elevation and that Fgf8 expression in the palate is Tbx1-dependent
机译：转录因子TBX1是与DiGeorge / Velocardiofacial综合征相关的发育异常的关键介质。小鼠研究表明，减少Tbx1的剂量会导致咽弓，心血管和颅面发育的缺陷。已深入研究了Tbx1在心脏发育中的作用。但是，通过研究Tbx1-/-小鼠，我们对它在pa发育中的作用了解得很少，我们发现了在pa伸长和升高的临界点期间存在缺陷。我们通过测量pa架子长度，增殖，凋亡，相关生长因子的表达以及pa融合试验中的变化来确定Tbx1-/-小鼠中固有的pa缺陷。 Tbx1-/-胚胎表现出c裂，其elevation升高失败率为100％，abnormal-口融合异常为50％。在Tbx1-/-小鼠中，pa的货架长度减少且舌头高度变大，表明了pa升高的物理障碍和并置。体外pa融合试验表明Tbx1-/-shelves架子具有融合能力，但辊式培养法表明无效的shelves架子不能延长Tbx1-/-pa架子中透明质酸的产生，这可能解释了elevation架子升高失败的原因。此外，在Tbx1-/-味觉中细胞增殖和凋亡受到干扰。在Tbx1-/-味觉架中检测到Fgf8表达急剧下降，这表明Fgf8依赖于味觉中的Tbx1。 Tbx1-/-shelves架子和舌头这些数据证明Tbx1是指导that伸长和升高的关键转录因子，F中的Fgf8表达是Tbx1依赖性的

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