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Abstract：
Organ formation requires precise regulation of cell cycle and morphogenetic events. Using the Drosophila embryonic salivary gland (SG) as a model, we uncover the role of the SP1/KLF transcription factor Huckebein (Hkb) in coordinating cell cycle regulation and morphogenesis. The hkb mutant SG exhibits defects in invagination positioning and organ size due to the abnormal death of SG cells. Normal SG development involves distal-to-proximal progression of endoreplication (endocycle), whereas hkb mutant SG cells undergo abnormal cell division, leading to cell death. Hkb represses the expression of key cell cycle and pro-apoptotic genes in the SG. Knockdown of cyclin E or cyclin-dependent kinase 1, or overexpression of fizzy-related rescues most of the morphogenetic defects observed in the hkb mutant SG. These results indicate that Hkb plays a critical role in controlling endoreplication by regulating the transcription of key cell cycle effectors to ensure proper organ formation.
摘要：
器官的形成需要精确调节细胞周期和形态发生事件。以果蝇胚胎唾液腺（SG）为模型，我们揭示了SP1/KLF转录因子Huckebein（Hkb）在协调细胞周期调控和形态发生中的作用。由于SG细胞的异常死亡，hkb突变体SG在内陷定位和器官大小方面表现出缺陷。正常的SG发育涉及内复制（内循环）的远端到近端进展，而hkb突变SG细胞经历异常细胞分裂，导致细胞死亡。Hkb抑制SG中关键细胞周期和促凋亡基因的表达。细胞周期蛋白E或细胞周期蛋白依赖性激酶1的敲低或与泡沫相关的过表达可以挽救hkb突变体SG中观察到的大多数形态发生缺陷。这些结果表明，Hkb通过调节关键细胞周期效应子的转录以确保适当的器官形成，在控制内复制中起着关键作用。
