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Mol. Cells 2009; 28(2): 93-98

Published online July 30, 2009

https://doi.org/10.1007/s10059-009-0105-0

© The Korean Society for Molecular and Cellular Biology

Overexpression of the Downward Leaf Curling
(DLC) Gene from Melon Changes Leaf Morphol-ogy
by Controlling Cell Size and Shape in Arabidopsis
Leaves

Jae-Jun Kee, Sang Eun Jun, Seung-A Baek, Tae-Soo Lee, Myung Rae Cho, Hyun-Sik Hwang,
Suk-Chan Lee, Jongkee Kim , Gyung-Tae Kim, and Kyung-Hoan Im

Received: April 30, 2009; Revised: June 10, 2009; Accepted: June 15, 2009

Abstract

A plant-specific gene was cloned from melon fruit. This gene was named downward leaf curling (CmDLC) based on the phenotype of transgenic Arabidopsis plants overexpressing the gene. This expression level of this gene was especially upregulated during melon fruit enlargement. Overexpression of CmDLC in Arabidopsis resulted in dwarfism and narrow, epinastically curled leaves. These phenotypes were found to be caused by a reduction in cell number and cell size on the adaxial and abaxial sides of the epidermis, with a greater reduction on the abaxial side of the leaves. These phenotypic characteristics, combined with the more wavy morphology of epidermal cells in overexpression lines, indicate that CmDLC overexpression affects cell elongation and cell morphology. To investigate intracellular protein localization, a CmDLC-GFP fusion protein was made and expressed in onion epidermal cells. This protein was observed to be preferentially localized close to the cell membrane. Thus, we report here a new plant-specific gene that is localized to the cell membrane and that controls leaf cell number, size and morphology.

Keywords Arabidopsis, cell size, CmDLC, epinasty, leaf morphology, melon

Article

Research Article

Mol. Cells 2009; 28(2): 93-98

Published online August 31, 2009 https://doi.org/10.1007/s10059-009-0105-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Overexpression of the Downward Leaf Curling
(DLC) Gene from Melon Changes Leaf Morphol-ogy
by Controlling Cell Size and Shape in Arabidopsis
Leaves

Jae-Jun Kee, Sang Eun Jun, Seung-A Baek, Tae-Soo Lee, Myung Rae Cho, Hyun-Sik Hwang,
Suk-Chan Lee, Jongkee Kim , Gyung-Tae Kim, and Kyung-Hoan Im

Received: April 30, 2009; Revised: June 10, 2009; Accepted: June 15, 2009

Abstract

A plant-specific gene was cloned from melon fruit. This gene was named downward leaf curling (CmDLC) based on the phenotype of transgenic Arabidopsis plants overexpressing the gene. This expression level of this gene was especially upregulated during melon fruit enlargement. Overexpression of CmDLC in Arabidopsis resulted in dwarfism and narrow, epinastically curled leaves. These phenotypes were found to be caused by a reduction in cell number and cell size on the adaxial and abaxial sides of the epidermis, with a greater reduction on the abaxial side of the leaves. These phenotypic characteristics, combined with the more wavy morphology of epidermal cells in overexpression lines, indicate that CmDLC overexpression affects cell elongation and cell morphology. To investigate intracellular protein localization, a CmDLC-GFP fusion protein was made and expressed in onion epidermal cells. This protein was observed to be preferentially localized close to the cell membrane. Thus, we report here a new plant-specific gene that is localized to the cell membrane and that controls leaf cell number, size and morphology.

Keywords: Arabidopsis, cell size, CmDLC, epinasty, leaf morphology, melon

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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