Rhomboid Enhancer Activity Defines a Subset of Drosophila Neural Precursors Required for Proper Feeding, Growth and Viability.
Rhomboid Enhancer Activity Defines a Subset of Drosophila Neural Precursors Required for Proper Feeding, Growth and Viability.
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DOI：
10.1371/journal.pone.0134915
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Gebelein B
中科院分区：
文献类型：
--
作者：
Gresser AL;Gutzwiller LM;Gauck MK;Hartenstein V;Cook TA;Gebelein B
有机体生长调节需要多种代谢、激素和神经通路的相互作用。虽然其中许多的分子基础是很好的特点，很少有人知道的发育起源的生长调节结构和机制控制进食和饱腹感。出于这些原因，需要新的工具和方法来将离散细胞群体的特化和成熟与其随后的调节作用联系起来。在这项研究中，我们描述了一个菱形增强子元件，选择性地标记四个果蝇胚胎神经前体。这些前体产生周围神经系统的下咽感觉器官和胚胎中枢神经系统中脑区域的神经元子集。胚胎发生后，菱形增强子在幼虫咽上皮内的细胞亚群中是活跃的。增强子靶向毒素的表达改变了感觉器官的形态，并导致幼虫生长受损、发育迟缓、前气门外翻缺陷和致死。限制毒素表达的持续时间揭示了这些影响的关键时期的差异。胚胎表达导致发育缺陷和部分渗透性蛹前致死。然而，胚胎表达的幸存者最终成为可存活的成年人。相反，胚胎后毒素表达导致完全渗透致死。为了更好地定义幼虫的生长缺陷，我们使用了各种测定来证明毒素靶向的幼虫能够定位、摄取和清除食物，并且它们表现出正常的食物搜索行为。然而，引人注目的是，在食物暴露后，这些幼虫显示出消费的快速减少，这表明与幼虫生长受损时期相关的饱腹感现象。总之，这些数据表明这些增强子定义的谱系在调节摄食、生长和生存力方面的关键作用。
Organismal growth regulation requires the interaction of multiple metabolic, hormonal and neuronal pathways. While the molecular basis for many of these are well characterized, less is known about the developmental origins of growth regulatory structures and the mechanisms governing control of feeding and satiety. For these reasons, new tools and approaches are needed to link the specification and maturation of discrete cell populations with their subsequent regulatory roles. In this study, we characterize a rhomboid enhancer element that selectively labels four Drosophila embryonic neural precursors. These precursors give rise to the hypopharyngeal sensory organ of the peripheral nervous system and a subset of neurons in the deutocerebral region of the embryonic central nervous system. Post embryogenesis, the rhomboid enhancer is active in a subset of cells within the larval pharyngeal epithelium. Enhancer-targeted toxin expression alters the morphology of the sense organ and results in impaired larval growth, developmental delay, defective anterior spiracle eversion and lethality. Limiting the duration of toxin expression reveals differences in the critical periods for these effects. Embryonic expression causes developmental defects and partially penetrant pre-pupal lethality. Survivors of embryonic expression, however, ultimately become viable adults. In contrast, post-embryonic toxin expression results in fully penetrant lethality. To better define the larval growth defect, we used a variety of assays to demonstrate that toxin-targeted larvae are capable of locating, ingesting and clearing food and they exhibit normal food search behaviors. Strikingly, however, following food exposure these larvae show a rapid decrease in consumption suggesting a satiety-like phenomenon that correlates with the period of impaired larval growth. Together, these data suggest a critical role for these enhancer-defined lineages in regulating feeding, growth and viability.