PTEN affects cell size, cell proliferation and apoptosis during Drosophila eye development

Author:

Huang H.1,Potter C.J.1,Tao W.1,Li D.M.1,Brogiolo W.1,Hafen E.1,Sun H.1,Xu T.1

Affiliation:

1. Howard Hughes Medical Institute and Department of Genetics, Yale University School of Medicine, Boyer Center for Molecular Medicine, New Haven, CT 06536-0812, USA.

Abstract

Mutations in the tumor suppressor gene PTEN (MMAC1/TEP1) are associated with a large number of human cancers and several autosomal-dominant disorders. Mice mutant for PTEN die at early embryonic stages and the mutant embryonic fibroblasts display decreased sensitivity to cell death. Overexpression of PTEN in different mammalian tissue culture cells affects various processes including cell proliferation, cell death and cell migration. We have characterized the Drosophila PTEN gene and present evidence that both inactivation and overexpression of PTEN affect cell size, while overexpression of PTEN also inhibits cell cycle progression at early mitosis and promotes cell death during eye development in a context-dependent manner. Furthermore, we have shown that PTEN acts in the insulin signaling pathway and all signals from the insulin receptor can be antagonized by either Drosophila or human PTEN, suggesting a potential means for alleviating symptoms associated with altered insulin signaling.

Publisher

The Company of Biologists

Subject

Developmental Biology,Molecular Biology

Reference49 articles.

1. Autonomous control of cell and organ size by CHICO, a Drosophila homolog of vertebrate IRS1-4.;Bohni;Cell,1999

2. Targeted gene expression as a means of altering cell fates and generating dominant phenotypes.;Brand;Development,1993

3. Frequent inactivation of PTEN/MMAC1 in primary prostate cancer.;Cairns;Cancer Res,1997

4. New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway.;Cantley;Proc. Natl. Acad. Sci. USA,1999

5. Suppression of tumorigenicity of glioblastoma cells by adenovirus-mediated MMAC1/PTEN gene transfer.;Cheney;Cancer Res,1998

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3