In flowering plants, tapetum degeneration is proposed to be triggered by a programmed cell death (PCD) process during late stages of pollen development; the PCD is thought to provide cellular contents supporting pollen wall formation and to allow the subsequent pollen release. However, the molecular basis regulating tapetum PCD in plants remains poorly understood. We report the isolation and characterization of a rice (Oryza sativa) male sterile mutant tapetum degeneration retardation (tdr), which exhibits degeneration retardation of the tapetum and middle layer as well as collapse of microspores. The TDR gene is preferentially expressed in the tapetum and encodes a putative basic helix-loop-helix protein, which is likely localized to the nucleus. More importantly, two genes, Os CP1 and Os c6, encoding a Cys protease and a protease inhibitor, respectively, were shown to be the likely direct targets of TDR through chromatin immunoprecipitation analyses and the electrophoretic mobility shift assay. These results indicate that TDR is a key component of the molecular network regulating rice tapetum development and degeneration.

Animals display stereotyped behavioral modifications during development, but little is known about how genes and neural circuits are regulated to turn on/off behaviors. Here we report that Drosophila neuropeptide F (dNPF), a human NPY homolog, coordinates larval behavioral changes during development. The brain expression of npf is high in larvae attracted to food, whereas its downregulation coincides with the onset of behaviors of older larvae, including food aversion, hypermobility, and cooperative burrowing. Loss of dNPF signaling in young transgenic larvae led to the premature display of behavioral phenotypes associated with older larvae. Conversely, dNPF overexpression in older larvae prolonged feeding, and suppressed hypermobility and cooperative burrowing behaviors. The dNPF system provides a new paradigm for studying the central control of cooperative behavior.

Alcohol is likely to affect neurons nonselectively, and the understanding of its action in the CNS requires elucidation of underlying neuronal circuits and associated cellular processes. We have identified a Drosophila signaling system, comprising neurons expressing neuropeptide F (NPF, a homolog of mammalian neuropeptide Y) and its receptor, NPFR1, that acutely mediates sensitivity to ethanol sedation. Flies deficient in NPF͞NPFR1 signaling showed decreased alcohol sensitivity, whereas those overexpressing NPF exhibited the opposite phenotype. Furthermore, controlled functional disruption of NPF or NPFR1 neurons in adults rapidly confers resistance to ethanol sedation. Finally, the NPF͞NPFR1 system selectively mediates sedation by ethanol vapor but not diethyl ether, indicating that the observed NPF͞NPFR1 activity reflects a specialized response to alcohol sedation rather than a general response to intoxication by sedative agents. Together, our results provide the molecular and neural basis for the strikingly similar alcohol-responsive behaviors between flies and mammals.acute ethanol response ͉ neuropeptide Y ͉ neuropeptide F receptor A lcohol, a widely abused drug, impacts the functioning of the CNS in diverse animals. The behavioral responses to acute alcohol exposure are remarkably similar among humans, rodents, and even fruit flies. Alcohol induces an excitatory state at lower concentrations but exerts a sedative effect at higher doses (1, 2). The current knowledge about how this drug impacts the functioning of the CNS is rather limited. Ethanol is highly soluble in both water and lipids, and is likely to act on neurons in a nonselective manner. However, the sensitivity of neurons in different neural circuits to this drug may vary greatly (3). Thus, elucidation of neuronal circuits and underlying molecular mechanisms essential for alcohol sensitivity is a prerequisite for understanding how alcohol interferes with the functioning of the CNS.Neuropeptides are a group of chemically diverse signal molecules implicated in modulating a broad spectrum of physiological processes and behaviors (4). Mammalian neuropeptide Y (NPY) is a 36 aa neuromodulator present abundantly in many regions of the CNS, and acts thorough a number of Y receptor subtypes (5). Mice lacking NPY or Y1 displayed increased ethanol consumption and resistance to alcohol sedation, whereas animals overexpressing NPY showed opposite behavioral phenotypes (6, 7). These results provide genetic evidence of a critical role of the NPY signaling system in acute ethanol response. However, the elucidation of the physiological role of the NPY system and the action sites has been difficult largely because of the complexity of mammalian models.NPY family molecules have been found in diverse organisms (8-10). Neuropeptide F (NPF) is the sole member of the NPY family in the Drosophila genome, and its action is mediated by G protein-coupled seven-transmembrane receptors related to mammalian NPY receptors (11). Both NPY and NPF are present prominently, although...

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