Sox Protein COG-2 Function in C. Elegans Organogenesis

Sox 蛋白 COG-2 在线虫器官发生中的功能

• 批准号: 0131287
• 负责人: Wendy Hanna-Rose
• 金额: $ 36万
• 依托单位: Pennsylvania State Univ University Park
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-03-01 至 2006-02-28
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0131287&HistoricalAwards=false
• 关键词: Sox; Protein; COG; Function; C.

0131287Hanna-RoseThe long-term goal of the Hanna-Rose laboratory is to elucidate the molecular mechanisms that direct organogenesis. The focus of the proposed research is a detailed investigation of the role of the cog-2 gene and of a specific cell-cell fusion in promoting proper attachment of the C. elegans uterus and vulva. cog?2 encodes a Sox (SRY-related HMG box) family transcription factor that is expressed in a specific cell of the uterus called the uterine seam cell (utse). The utse normally executes a developmentally programmed cell fusion to another gonadal cell called the anchor cell. This cell-cell fusion promotes formation of an open channel between the uterus and the vulva in a late stage of organogenesis. In the absence of cog-2 function, utse cell fate is induced but fusion to the anchor cell (AC) is not executed. The aims of the proposed research are to determine whether COG-2 acts to regulate fusion directly or affects fusion indirectly through an effect on utse cell fate, to identify and characterize additional genes involved in AC-utse fusion, and to identify COG-2 binding partners. Results are expected to elucidate mechanisms whereby COG-2 functions. This will also shed light on potential regulatory targets for vertebrate Sox proteins. Furthermore, the results are expected to increase our understanding of how the formation of a proper connection between two organs is genetically programmed and to promote the development of tools for probing the mechanism of cell fusion.

0131287 Hanna-Rose Hanna-Rose实验室的长期目标是阐明指导器官发生的分子机制。这项研究的重点是详细研究cog-2基因和特定的细胞-细胞融合在促进C.子宫和外阴。齿轮？2编码Sox（SRY相关HMG盒）家族转录因子，该转录因子在称为子宫缝细胞（utse）的子宫特定细胞中表达。 utse通常执行发育程序细胞融合到另一个性腺细胞称为锚细胞。 这种细胞-细胞融合在器官发生的后期促进子宫和外阴之间开放通道的形成。 在缺乏cog-2功能的情况下，utse细胞命运被诱导，但不执行与锚细胞（AC）的融合。 拟议研究的目的是确定COG-2是否直接调节融合或通过对utse细胞命运的影响间接影响融合，以鉴定和表征参与AC-utse融合的其他基因，并鉴定COG-2结合伴侣。 结果有望阐明COG-2发挥作用的机制。 这也将揭示脊椎动物Sox蛋白的潜在调控靶点。 此外，这些结果有望增加我们对两个器官之间正确连接的形成是如何遗传编程的理解，并促进探索细胞融合机制的工具的开发。