title: The Nuclear Matrix Protein Megator Regulates Stem Cell Asymmetric Division through the Mitotic Checkpoint Complex in Drosophila Testes.
abstract: In adult Drosophila testis, asymmetric division of germline stem cells (GSCs) is specified by an oriented spindle and cortically localized adenomatous coli tumor suppressor homolog 2 (Apc2). However, the molecular mechanism underlying these events remains unclear. Here we identified Megator (Mtor), a nuclear matrix protein, which regulates GSC maintenance and asymmetric division through the spindle assembly checkpoint (SAC) complex. Loss of Mtor function results in Apc2 mis-localization, incorrect centrosome orientation, defective mitotic spindle formation, and abnormal chromosome segregation that lead to the eventual GSC loss. Expression of mitotic arrest-deficient-2 (Mad2) and monopolar spindle 1 (Mps1) of the SAC complex effectively rescued the GSC loss phenotype associated with loss of Mtor function. Collectively our results define a new role of the nuclear matrix-SAC axis in regulating stem cell maintenance and asymmetric division.
authors.affiliation: The Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States of America.
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.affiliation: The Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States of America.
authors.forename: Shree Ram
authors.initials: SR
authors.lastname: Singh
authors.affiliation: The Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States of America.
authors.forename: Xiankun
authors.initials: X
authors.lastname: Zeng
authors.affiliation: The Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States of America.
authors.forename: Jiangsha
authors.initials: J
authors.lastname: Zhao
authors.affiliation: The Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States of America.
authors.forename: Steven X
authors.initials: SX
authors.lastname: Hou
mesh_terms: D000818:Animals; D060049:Asymmetric Cell Division; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D018385:Centrosome / Q000378:metabolism; D020090:Chromosome Segregation; D004330:Drosophila / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism*; D059566:M Phase Cell Cycle Checkpoints; D064246:Mad2 Proteins / Q000235:genetics / Q000378:metabolism; D008297:Male; D034521:Nuclear Matrix-Associated Proteins / Q000235:genetics / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D013234:Stem Cells / Q000378:metabolism* / Q000502:physiology; D013737:Testis / Q000166:cytology / Q000378:metabolism*; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: C467323:APC2 protein, Drosophila; D018797:Cell Cycle Proteins; D029721:Drosophila Proteins; D064246:Mad2 Proteins; C577685:Mad2 protein, Drosophila; C498867:Mtor protein, Drosophila; D034521:Nuclear Matrix-Associated Proteins; D025521:Tumor Suppressor Proteins; C501876:Mps1 protein, Drosophila; D017346:Protein Serine-Threonine Kinases