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Mol. Cells 2010; 30(3): 255-262

Published online August 23, 2010

https://doi.org/10.1007/s10059-010-0116-x

© The Korean Society for Molecular and Cellular Biology

Calcineurin Regulates Coelomocyte Endocytosis via DYN-1 and CUP-4 in Caenorhabditis elegans

Hyun-Ok Song1, Jungsoo Lee1,4, Yon Ju Ji1,5, Meenakshi Dwivedi1, Jeong Hoon Cho2, Byung-Jae Park3, and Joohong Ahnn1,*

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1Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 133-791, Korea, 2Division of Biology Education, College of Education, Chosun University, Gwangju 501-759, Korea, 3Department of Life Science, Hallym University, Chunchon 200-702, Korea, 4Present address: Ernest Gallo Clinic and Research Center, Department of Neurology, Programs in Neuroscience and Biomedical Science, University of California, San Francisco, California 94608, USA, 5Present address: Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick, Maryland 21702, USA

Correspondence to : *Correspondence: joohong@hanyang.ac.kr

Received: April 28, 2010; Revised: May 30, 2010; Accepted: June 1, 2010

Abstract

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C. elegans coelomocytes are macrophage-like scavenger cells that provide an excellent in vivo system for the study of clathrin-mediated endocytosis. Using this in vivo system, several genes involved in coelomocyte endocytosis have been identified previously. However, the detailed mechanism of endocytic pathway is still unknown. Here, we report a new function of calcineurin, an evolutionarily conserved Ca2+/calmodulin-dependent Ser/Thr protein phos- phatase, in coelomocyte endocytosis. We found that calcineurin mutants show defective coelomocyte endocytosis. Genetic analysis suggests that calcineurin and a GTPase, dynamin (DYN-1), may function upstream of an orphan receptor, CUP-4, to regulate endocytosis. Therefore, we propose a model in which calcineurin may regulate coelomocyte endocytosis via DYN-1 and CUP-4 in C. elegans.

Keywords Ca2+ signaling, C. elegans, endocytosis, phosphatase

Article

Research Article

Mol. Cells 2010; 30(3): 255-262

Published online September 30, 2010 https://doi.org/10.1007/s10059-010-0116-x

Copyright © The Korean Society for Molecular and Cellular Biology.

Calcineurin Regulates Coelomocyte Endocytosis via DYN-1 and CUP-4 in Caenorhabditis elegans

Hyun-Ok Song1, Jungsoo Lee1,4, Yon Ju Ji1,5, Meenakshi Dwivedi1, Jeong Hoon Cho2, Byung-Jae Park3, and Joohong Ahnn1,*

1Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 133-791, Korea, 2Division of Biology Education, College of Education, Chosun University, Gwangju 501-759, Korea, 3Department of Life Science, Hallym University, Chunchon 200-702, Korea, 4Present address: Ernest Gallo Clinic and Research Center, Department of Neurology, Programs in Neuroscience and Biomedical Science, University of California, San Francisco, California 94608, USA, 5Present address: Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick, Maryland 21702, USA

Correspondence to:*Correspondence: joohong@hanyang.ac.kr

Received: April 28, 2010; Revised: May 30, 2010; Accepted: June 1, 2010

Abstract

C. elegans coelomocytes are macrophage-like scavenger cells that provide an excellent in vivo system for the study of clathrin-mediated endocytosis. Using this in vivo system, several genes involved in coelomocyte endocytosis have been identified previously. However, the detailed mechanism of endocytic pathway is still unknown. Here, we report a new function of calcineurin, an evolutionarily conserved Ca2+/calmodulin-dependent Ser/Thr protein phos- phatase, in coelomocyte endocytosis. We found that calcineurin mutants show defective coelomocyte endocytosis. Genetic analysis suggests that calcineurin and a GTPase, dynamin (DYN-1), may function upstream of an orphan receptor, CUP-4, to regulate endocytosis. Therefore, we propose a model in which calcineurin may regulate coelomocyte endocytosis via DYN-1 and CUP-4 in C. elegans.

Keywords: Ca2+ signaling, C. elegans, endocytosis, phosphatase

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.
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