Distinct Rac activation pathways control C. elegans cell migration and axon outgrowth

• Main Authors: Ting-Wen Cheng, 鄭婷文
• Other Authors: Yi-Chun Wu
• Format: Others
• Language: zh-TW
• Published: 2002
• Online Access: http://ndltd.ncl.edu.tw/handle/63280425710643656488

碩士 === 國立臺灣大學 === 動物學研究所 === 90 === Rac GTPases are involved in cytoskeletal rearrangement and act as molecular switch in various morphogenic events. However, the regulation of their activities during the development of multicellular organisms is not well understood. ced-10 and mig-2 are members of Rac GTPase family in C. elegans. A strong ced-10 mutation causes the uncoordinated phenotype while the null mutation in mig-2 does not have a strong influence in neuronal development in general. To understand roles of ced-10 and mig-2 and identify their respective upstream regulators during neuronal development we have undertaken genetic approaches and analyzed their functions in the development of specific motor and sensory neurons. We showed that ced-10 and mig-2 act redundantly to control P cell migration and the axon outgrowth of D type motoneurons. These two Rac GTPases also control amphid axon outgrowth in a redundant fashion but their activities are not required for the amphid dendrite formation. Our genetic data indicate that unc-73, which encodes a protein related to Trio-like guanine nucleotide exchange factor, acts as an activator of ced-10 and mig-2 during P cell migration and axon outgrowth of D type motoneurons and amphid sensory neurons. Furthermore, rac regulators ced-2/crkII and ced-5/dock180 that function upstream of ced-10 during DTC migration and cell-corpse engulfment act genetically upstream of ced-10 and mig-2 during axon outgrowth of D-type motor neurons and appear to act on mig-2 rather than ced-10 during P cell migration. However, neither ced-2/crkII nor ced-5/dock180 is involved in amphid axon outgrowth. Therefore, distinct rac regulators control ced-10 and mig-2 differentially in various cellular processes.