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Mol. Cells 2012; 34(4): 367-374

Published online September 6, 2012

https://doi.org/10.1007/s10059-012-0111-5

© The Korean Society for Molecular and Cellular Biology

Overexpression of a LAM Domain Containing RNA-Binding Protein LARP1c Induces Precocious Leaf Senescence in Arabidopsis

Bangyue Zhang, Jianheng Jia, Min Yang, Chunxia Yan, and Yuzhen Han*

State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China

Correspondence to : *Correspondence: hanyuzhen@cau.edu.cn

Received: April 13, 2012; Revised: July 11, 2012; Accepted: July 26, 2012

Abstract

Leaf senescence is the final stage of leaf life history, and it can be regulated by multiple internal and external cues. La-related proteins (LARPs), which contain a well-con-served La motif (LAM) domain and normally a canonical RNA recognition motif (RRM) or noncanonical RRM-like motif, are widely present in eukaryotes. Six LARP genes (LARP1a-1c and LARP6a-6c) are present in Arabidopsis, but their biological functions have not been studied previously. In this study, we investigated the biological roles of LARP1c from the LARP1 family. Constitutive or inducible overexpression of LARP1c caused premature leaf senescence. Expression levels of several senes-cence-asso-ciated genes and defense-related genes were elevated upon overexpression of LARP1c. The LARP1c null mutant 1c-1 impaired ABA-, SA-, and MeJA-induced leaf senescence in detached leaves. Gene expression profiles of LARP1c showed age-dependent expression in rosette leaves. Taken together, our results suggest LARP1c is involved in regulation of leaf senescence.

Keywords Arabidopsis, LARP1c, senescence, senescence-associated genes

Article

Research Article

Mol. Cells 2012; 34(4): 367-374

Published online October 31, 2012 https://doi.org/10.1007/s10059-012-0111-5

Copyright © The Korean Society for Molecular and Cellular Biology.

Overexpression of a LAM Domain Containing RNA-Binding Protein LARP1c Induces Precocious Leaf Senescence in Arabidopsis

Bangyue Zhang, Jianheng Jia, Min Yang, Chunxia Yan, and Yuzhen Han*

State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China

Correspondence to:*Correspondence: hanyuzhen@cau.edu.cn

Received: April 13, 2012; Revised: July 11, 2012; Accepted: July 26, 2012

Abstract

Leaf senescence is the final stage of leaf life history, and it can be regulated by multiple internal and external cues. La-related proteins (LARPs), which contain a well-con-served La motif (LAM) domain and normally a canonical RNA recognition motif (RRM) or noncanonical RRM-like motif, are widely present in eukaryotes. Six LARP genes (LARP1a-1c and LARP6a-6c) are present in Arabidopsis, but their biological functions have not been studied previously. In this study, we investigated the biological roles of LARP1c from the LARP1 family. Constitutive or inducible overexpression of LARP1c caused premature leaf senescence. Expression levels of several senes-cence-asso-ciated genes and defense-related genes were elevated upon overexpression of LARP1c. The LARP1c null mutant 1c-1 impaired ABA-, SA-, and MeJA-induced leaf senescence in detached leaves. Gene expression profiles of LARP1c showed age-dependent expression in rosette leaves. Taken together, our results suggest LARP1c is involved in regulation of leaf senescence.

Keywords: Arabidopsis, LARP1c, senescence, senescence-associated genes

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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