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Mol. Cells 2012; 34(5): 413-423

Published online July 6, 2012

https://doi.org/10.1007/s10059-012-0098-y

© The Korean Society for Molecular and Cellular Biology

Genes for Plant Autophagy: Functions and Interactions

Soon-Hee Kim, Chian Kwon1, Jae-Hoon Lee2, and Taijoon Chung*

Department of Biological Sciences, Pusan National University, Busan 609-735, Korea, 1Department of Molecular Biology, Brain Korea 21 Graduate Program for RNA Biology, Dankook University, Yongin 448-701, Korea, 2Department of Biological Education, Pusan National University, Busan 609-735, Korea

Correspondence to : *Correspondence: taijoon@pusan.ac.kr

Received: April 13, 2014; Revised: May 22, 2012; Accepted: May 23, 2012

Abstract

Autophagy, or self-consuming of cytoplasmic constitu-ents in a lytic compartment, plays a crucial role in nutrient recycling, development, cell homeostasis, and defense against pathogens and toxic products. Autophagy in plant cells uses a conserved machinery of core Autophagy-related (Atg) proteins. Recently, research on plant auto-phagy has been expanding and other components inter-acting with the core Atg proteins are being revealed. In addition, growing evidence suggests that autophagy communicates with other cellular pathways such as the ubiquitin-proteasome system, protein secretory pathway, and endocytic pathway. An increase in our understanding of plant autophagy will undoubtedly help test the hypothesized functions of plant autophagy in programmed cell death, vacuole biogenesis, and responses to biotic, abiotic, and nutritional stresses. In this review, we summarize recent progress on these topics and suggest topics for future research, after in-specting common phenotypes of current Arabidopsis atg mutants.

Keywords autophagosome, NBR1, p62, selective autophagy

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Mol. Cells 2012; 34(5): 413-423

Published online November 30, 2012 https://doi.org/10.1007/s10059-012-0098-y

Copyright © The Korean Society for Molecular and Cellular Biology.

Genes for Plant Autophagy: Functions and Interactions

Soon-Hee Kim, Chian Kwon1, Jae-Hoon Lee2, and Taijoon Chung*

Department of Biological Sciences, Pusan National University, Busan 609-735, Korea, 1Department of Molecular Biology, Brain Korea 21 Graduate Program for RNA Biology, Dankook University, Yongin 448-701, Korea, 2Department of Biological Education, Pusan National University, Busan 609-735, Korea

Correspondence to:*Correspondence: taijoon@pusan.ac.kr

Received: April 13, 2014; Revised: May 22, 2012; Accepted: May 23, 2012

Abstract

Autophagy, or self-consuming of cytoplasmic constitu-ents in a lytic compartment, plays a crucial role in nutrient recycling, development, cell homeostasis, and defense against pathogens and toxic products. Autophagy in plant cells uses a conserved machinery of core Autophagy-related (Atg) proteins. Recently, research on plant auto-phagy has been expanding and other components inter-acting with the core Atg proteins are being revealed. In addition, growing evidence suggests that autophagy communicates with other cellular pathways such as the ubiquitin-proteasome system, protein secretory pathway, and endocytic pathway. An increase in our understanding of plant autophagy will undoubtedly help test the hypothesized functions of plant autophagy in programmed cell death, vacuole biogenesis, and responses to biotic, abiotic, and nutritional stresses. In this review, we summarize recent progress on these topics and suggest topics for future research, after in-specting common phenotypes of current Arabidopsis atg mutants.

Keywords: autophagosome, NBR1, p62, selective autophagy

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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