权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

HORMONAL REGULATION OF THE INSECT EPIDERMIS

昆虫表皮的激素调节

基本信息

批准号：
2633416
负责人：
LYNN M RIDDIFORD
金额：
$ 25.79万
依托单位：
UNIVERSITY OF WASHINGTON
依托单位国家：
美国
项目类别：
财政年份：
1979
资助国家：
美国
起止时间：
1979-01-01 至 1998-12-31
项目状态：
已结题

项目摘要

Our long-term goal is to understand how ecdysteroids and juvenile hormone (JH) act to coordinate insect growth and development. Ecdysteroids cause molting, both suppressing on-going intermolt gene expression and activating the cascade of genes necessary for the molt. Moreover, ecdysteroids are important for maintenance of tissue synchrony during the molt. JH determines whether the molt will be progressive or not; in its presence metamorphosis cannot occur. Thus, JH prevents ecdysteroid's activation of previously unexpressed genes that allow the cell to change its differentiated state. Our model for studying this action is the insect epidermis which makes the cuticle, i.e. the exoskeleton, and which is a single cell layer thick and can readily be cultured. Our specific aims for the next 5 years are: 1) To characterize the regulatory regions of the several larval cuticular genes and dopa decarboxylase and to study their possible interactions with ecdysteroid and JH receptors and/or the transcription factors that these hormones induce. 2) To clone, characterize, and study the hormonal control of a pupal-specific cuticle gene to complete our arsenal of epidermal genes that are hormonally regulated at metamorphosis. 3) To determine the role in molting and metamorphosis of the ecdysteroid-induced transcription factor ("RAR") that shows significant similarity to the mammalian retinoic acid receptor. 4) To examine possible changes in EcR subtypes in the epidermis through larval molting and metamorphosis by in situ hybridization and immunocytochemistry and how they are regulated by the hormonal milieu. These studies will allow us to define at the molecular level how ecdysteroids and JH regulate insect growth, molting, and metamorphosis. This information can lead to design of new types of insect growth regulators essential to the control of disease vectors. Also, emerging similarities between the actions of JH and of retinoic acid in the regulation of cell differentiation, particularly in mammalian epidermis, make the insect epidermis a possible nonvertebrate model for study of common mechanisms involved.

我们的长期目标是了解蜕皮激素和保幼激素 (JH)协调昆虫的生长和发育。蜕皮激素导致蜕皮，既抑制正在进行的蜕皮基因表达，又激活蜕皮所需的一连串基因此外，蜕皮类固醇是对于在蜕皮期间保持组织同步很重要。 JH 决定是否蜕皮将是渐进或不;在其存在变形是不会发生的。因此，JH阻止蜕皮激素激活以前未表达的基因，使细胞改变其差异化国家我们研究这种行为的模型是昆虫表皮，使角质层，即外骨骼，这是一个单细胞层厚并且可以容易地培养。我们的具体目标是未来5年的目标是：1）确定几个幼虫表皮基因和多巴脱羧酶，并研究其可能与蜕皮激素和JH受体和/或这些激素诱导的转录因子。 2)为了克隆，描述和研究蛹特定角质层的激素控制基因来完善我们的表皮基因库，在变态时受到调节。 3)为了确定在蜕皮中的作用，蜕皮激素诱导的转录因子（“RAR”）的变态，显示出与哺乳动物视黄酸受体的显著相似性。四、为了研究幼虫表皮中EcR亚型的可能变化，蜕皮和变态的原位杂交和免疫细胞化学以及它们是如何受荷尔蒙环境的调节。这些研究将使我们能够在分子水平上确定蜕皮激素和JH如何调节昆虫的生长、蜕皮和变态。这些信息可能导致设计控制害虫所必需的新型昆虫生长调节剂病媒此外，JH的行为和视黄酸在调节细胞分化中的作用，哺乳动物的表皮，使昆虫表皮成为可能的非脊椎动物用于研究所涉及的共同机制的模型。