ArticleDevelopmental biology2012
Sgt1 acts via an LKB1/AMPK pathway to establish cortical polarity in larval neuroblasts.
Article in Developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- SUGT1 is a prognostic biomarker and is associated with immune infiltrates in ovarian cancer.European journal of medical research · 2025Article
- SUGT1 regulates the progression of ovarian cancer through the AKT/PI3K/mTOR signaling pathway.Translational oncology · 2024Article
- Identification of protein quality control regulators using a Drosophila model of TPI deficiency.Neurobiology of disease · 2021Article
- Mutations in ANKLE2, a ZIKA Virus Target, Disrupt an Asymmetric Cell Division Pathway in Drosophila Neuroblasts to Cause Microcephaly.Developmental cell · 2019Article
- Hsp83/Hsp90 Physically Associates with Insulin Receptor to Promote Neural Stem Cell Reactivation.Stem cell reports · 2018Article
- Cardiac Phosphodiesterases and Their Modulation for Treating Heart Disease.Handbook of experimental pharmacology · 2017Review
- LKB1 deletion causes early changes in atrial channel expression and electrophysiology prior to atrial fibrillation.Cardiovascular research · 2015Article
- The mucolipidosis IV Ca2+ channel TRPML1 (MCOLN1) is regulated by the TOR kinase.The Biochemical journal · 2015Article
- Differential control of Yorkie activity by LKB1/AMPK and the Hippo/Warts cascade in the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The oncogenic role of the cochaperone Sgt1.Oncogenesis · 2015Article
- Isolation of AMP-activated protein kinase (AMPK) alleles required for neuronal maintenance in Drosophila melanogaster.Biology open · 2013Article
- Drosophila melanogaster: a model and a tool to investigate malignancy and identify new therapeutics.Nature reviews. Cancer · 2013Review
- Caenorhabditis elegans PIG-1/MELK acts in a conserved PAR-4/LKB1 polarity pathway to promote asymmetric neuroblast divisions.Genetics · 2013Article
- The Snail family member Worniu is continuously required in neuroblasts to prevent Elav-induced premature differentiation.Developmental cell · 2012Article
- Scrib regulates HGF-mediated epithelial morphogenesis and is stabilized by Sgt1-HSP90.Journal of cell science · 2012Article
- The Role of AMPK in Drosophila melanogaster.Experientia supplementum (2012)Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Drosophila neuroblasts are a model system for studying stem cell self-renewal and the establishment of cortical polarity. Larval neuroblasts generate a large apical self-renewing neuroblast, and a small basal cell that differentiates. We performed a genetic screen to identify regulators of neuroblast self-renewal, and identified a mutation in sgt1 (suppressor-of-G2-allele-of-skp1) that had fewer neuroblasts. We found that sgt1 neuroblasts have two polarity phenotypes: failure to establish apical cortical polarity at prophase, and lack of cortical Scribble localization throughout the cell cycle. Apical cortical polarity was partially restored at metaphase by a microtubule-induced cortical polarity pathway. Double mutants lacking Sgt1 and Pins (a microtubule-induced polarity pathway component) resulted in neuroblasts without detectable cortical polarity and formation of "neuroblast tumors." Mutants in hsp83 (encoding the predicted Sgt1-binding protein Hsp90), LKB1, or AMPKα all show similar prophase apical cortical polarity defects (but no Scribble phenotype), and activated AMPKα rescued the sgt1 mutant phenotype. We propose that an Sgt1/Hsp90-LKB1-AMPK pathway acts redundantly with a microtubule-induced polarity pathway to generate neuroblast cortical polarity, and the absence of neuroblast cortical polarity can produce neuroblast tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.