دورية أكاديمية

Ras promotes germline stem cell division in Drosophila ovaries.

التفاصيل البيبلوغرافية
العنوان: Ras promotes germline stem cell division in Drosophila ovaries.
المؤلفون: Zhang Q; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Wang Y; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Bu Z; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Zhang Y; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Zhang Q; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Li L; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Yan L; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Wang Y; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China., Zhao S; Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, People's Republic of China. Electronic address: swzhao@nankai.edu.cn.
المصدر: Stem cell reports [Stem Cell Reports] 2024 Aug 13; Vol. 19 (8), pp. 1205-1216. Date of Electronic Publication: 2024 Jul 18.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101611300 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2213-6711 (Electronic) Linking ISSN: 22136711 NLM ISO Abbreviation: Stem Cell Reports Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, c 2013-
مواضيع طبية MeSH: Ovary*/cytology , Ovary*/metabolism , Drosophila Proteins*/metabolism , Drosophila Proteins*/genetics , ras Proteins*/metabolism , ras Proteins*/genetics , Cell Division*, Animals ; Female ; Drosophila melanogaster/cytology ; Drosophila melanogaster/metabolism ; Drosophila melanogaster/genetics ; MAP Kinase Signaling System ; Germ Cells/metabolism ; Germ Cells/cytology ; Stem Cells/metabolism ; Stem Cells/cytology ; Mitosis ; Drosophila/metabolism ; Signal Transduction
مستخلص: The Ras family genes are proto-oncogenes that are highly conserved from Drosophila to humans. In Drosophila, Ras V12 is a constitutively activated form of the Ras oncoprotein, and its function in cell-cycle progression is context dependent. However, how it influences the cell cycle of female germline stem cells (GSCs) still remains unknown. Using both wild-type GSCs and bam mutant GSC-like cells as model systems, here we determined that Ras V12 overexpression promotes GSC division, not growth, opposite to that in somatic wing disc cells. Ras performs this function through activating the mitogen-activated protein kinase (MAPK) signaling. This signaling is activated specifically in the M phase of mitotic germ cells, including both wild-type GSCs and bam mutant GSC-like cells. Furthermore, Ras V12 overexpression triggers polyploid nurse cells to die through inducing mitotic stress. Given the similarities between Drosophila and mammalian GSCs, we propose that the Ras/MAPK signaling also promotes mammalian GSC division.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
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فهرسة مساهمة: Keywords: Drosophila; MAPK; Ras; bam; germline stem cell
المشرفين على المادة: 0 (Drosophila Proteins)
EC 3.6.5.2 (ras Proteins)
تواريخ الأحداث: Date Created: 20240719 Date Completed: 20240814 Latest Revision: 20240906
رمز التحديث: 20240906
مُعرف محوري في PubMed: PMC11368681
DOI: 10.1016/j.stemcr.2024.06.005
PMID: 39029459
قاعدة البيانات: MEDLINE
الوصف
تدمد:2213-6711
DOI:10.1016/j.stemcr.2024.06.005