The role of PRL during sea urchin development

碩士 === 國立臺灣海洋大學 === 生物科技研究所 === 100 === The phosphatase of regenerating liver (PRL) family, consisting of PRL-1, PRL-2, and PRL-3 in human, represents a group of phosphatases related to tumorigenesis. PRL family plays critical roles in the processes of tumor initiation and development, such as cance...

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Bibliographic Details
Main Authors: Han-Ru Li, 李函儒
Other Authors: Yi-Hsien Su
Format: Others
Language:zh-TW
Published: 2012
Online Access:http://ndltd.ncl.edu.tw/handle/09429761193999483039
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Summary:碩士 === 國立臺灣海洋大學 === 生物科技研究所 === 100 === The phosphatase of regenerating liver (PRL) family, consisting of PRL-1, PRL-2, and PRL-3 in human, represents a group of phosphatases related to tumorigenesis. PRL family plays critical roles in the processes of tumor initiation and development, such as cancer cell invasion, migration, angiogenesis, and metastasis. However, the role of PRL during development is unclear. Sea urchin embryos have been a research model for studying cell behaviors and morphogenesis because of its simple organization that are easily observed. Blocking the expression of several phosphatases in the sea urchin embryo has been shown to interfere with the formation of endomesoderm including skeletogenesis. In this study, I identified sea urchin PRL and studied its function during embryogenesis. Sea urchin contains a single PRL gene (SpPRL) that encodes for a 174-aa protein with high similarity to its human homologs. SpPRL is expressed maternally and ubiquitously during development, and proteins are localized dominantly in secondary mesenchyme cells (SMCs) after the mesenchyme blastula stage. In SpPRL-knockdown and hPRL-3 inhibitor-treated embryos, the formation of the embryonic skeleton was affected and the morphology of pigment cells was abnormal. The expression levels of several primary mesenchyme cell (PMC, skeletogenic lineage cells) differentiation and specification genes were declined in SpPRL knockdown embryos. Therefore, I proposed that SpPRL affects skeletogenesis through interactions between SMCs and PMCs.