ArticleMolecular biology of the cell2016
Heparan sulfate regulates the number and centrosome positioning of Drosophila male germline stem cells.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Heparan sulfate inhibits transforming growth factor β signaling and functions in cis and in trans to regulate prostate stem/progenitor cell activities.Glycobiology · 2020Article
- Functional analysis of glycosylation using Drosophila melanogaster.Glycoconjugate journal · 2020Review
- Regulation of Drosophila germline stem cells.Current opinion in cell biology · 2019Review
- Review
- Establishment and characterization of Drosophila cell lines mutant for heparan sulfate modifying enzymes.Glycobiology · 2019Article
- Loss of heparan sulfate in the niche leads to tumor-like germ cell growth in the Drosophila testis.Glycobiology · 2018Article
- Article
- Role of Hippo Pathway Effector Tafazzin Protein in Maintaining Stemness of Umbilical Cord-Derived Mesenchymal Stem Cells (UC-MSC).International journal of hematology-oncology and stem cell research · 2018Article
- Regulation of neuroblast proliferation by surface glia in the Drosophila larval brain.Scientific reports · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Stem cell division is tightly controlled via secreted signaling factors and cell adhesion molecules provided from local niche structures. Molecular mechanisms by which each niche component regulates stem cell behaviors remain to be elucidated. Here we show that heparan sulfate (HS), a class of glycosaminoglycan chains, regulates the number and asymmetric division of germline stem cells (GSCs) in the Drosophila testis. We found that GSC number is sensitive to the levels of 6-O sulfate groups on HS. Loss of 6-O sulfation also disrupted normal positioning of centrosomes, a process required for asymmetric division of GSCs. Blocking HS sulfation specifically in the niche, termed the hub, led to increased GSC numbers and mispositioning of centrosomes. The same treatment also perturbed the enrichment of Apc2, a component of the centrosome-anchoring machinery, at the hub-GSC interface. This perturbation of the centrosome-anchoring process ultimately led to an increase in the rate of spindle misorientation and symmetric GSC division. This study shows that specific HS modifications provide a novel regulatory mechanism for stem cell asymmetric division. The results also suggest that HS-mediated niche signaling acts upstream of GSC division orientation control.
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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.