KIN-29 SIK SIGNALING THE THEREGULATION OF FOOD-RELATED BEHAVIORS & DEVELOPMENT

KIN-29 SIK 发出食品相关行为监管信号

基本信息

  • 批准号:
    8360612
  • 负责人:
  • 金额:
    $ 18.39万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2011
  • 资助国家:
    美国
  • 起止时间:
    2011-06-01 至 2012-05-31
  • 项目状态:
    已结题

项目摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Growth, and ultimately the size of an animal is regulated by the nervous system, which integrates genetically hardwired developmental processes together with the plastic process of continuous sensing of an animal's environmental condition and energy state. When growth or energy states are deregulated in humans, disorders such as cancer or obesity can result. How sensory inputs and integration of environmental information by the nervous system influences growth is poorly understood. C. elegans provides a tractable system for defining the molecular and neural basis of body size. C. elegans body size is partly regulated by sensory perception and food signals, suggesting that the sensory system regulates body size in response to changing environmental conditions. Our previous work demonstrates that the KIN-29 Salt-Inducible Kinase (SIK) pathways acts in the chemosensory neurons (CNs) to regulate sensory gene expression, body size and food-related behaviors. We postulate that correct regulation of sensory gene expression is necessary to appropriately acquire environmental signals, thereby regulating sensory inputs into pathways important for body size. SIK function is involved in feeding/fasting responses, and is a regulator of the TGFbeta pathway implicated in growth control in both mammals and in C. elegans. Conservation of SIK function from humans to C. elegans offers the opportunity to explore how sensory information may be involved in cell growth and body size. We use genetic and genomic approaches in C. elegans to propose the following: Aim 1) to define the subset(s) of sensory neurons that regulate body size via KIN-29; Aim 2) define the complete set of sensory genes regulated by KIN-29; and Aim 3) to identify novel genes acting in the KIN-29-mediated body size pathway. The study of conserved biological pathways in C. elegans will inform our understanding of human pathways involved in health and disease.
这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的, 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量, 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 动物的生长和最终的大小是由神经系统调节的,神经系统将遗传上的硬连线发育过程与连续感知动物环境条件和能量状态的可塑性过程结合在一起。当人类的生长或能量状态失调时,可能会导致癌症或肥胖等疾病。感觉输入和神经系统对环境信息的整合如何影响生长还知之甚少。C.秀丽线虫提供了一个易于处理的系统来定义身体大小的分子和神经基础。C.秀丽线虫的身体大小部分受感官知觉和食物信号的调节,这表明感觉系统响应变化的环境条件来调节身体大小。我们的前期工作表明,KIN-29盐诱导激酶(SIK)通路在化学感觉神经元(CN)中起作用,调节感觉基因表达、身体大小和食物相关行为。我们假设,正确的调控感觉基因的表达是必要的,以适当地获取环境信号,从而调节感官输入到身体大小的重要途径。在哺乳动物和C.优美的从人到C.线虫提供了探索感觉信息如何参与细胞生长和身体大小的机会。我们使用遗传和基因组方法在C。elegans提出以下目标:目的1)定义通过KIN-29调节身体大小的感觉神经元的子集;目的2)定义由KIN-29调节的感觉基因的完整集合;以及目的3)鉴定在KIN-29介导的身体大小途径中起作用的新基因。对C.秀丽隐杆线虫将为我们了解人类健康和疾病的途径提供信息。

项目成果

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ALEXANDER VAN DER LINDEN其他文献

ALEXANDER VAN DER LINDEN的其他文献

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{{ truncateString('ALEXANDER VAN DER LINDEN', 18)}}的其他基金

KIN-29 SIK SIGNALING THE THEREGULATION OF FOOD-RELATED BEHAVIORS & DEVELOPMENT
KIN-29 SIK 发出食品相关行为监管信号
  • 批准号:
    8168235
  • 财政年份:
    2010
  • 资助金额:
    $ 18.39万
  • 项目类别:

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