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First published online November 26, 2008; 10.1104/pp.108.127415

Plant Physiology 149:816-824 (2009)
© 2009 American Society of Plant Biologists

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DEVELOPMENT AND HORMONE ACTION

InPSR26, a Putative Membrane Protein, Regulates Programmed Cell Death during Petal Senescence in Japanese Morning Glory1,[W],[OA]

Kenichi Shibuya*, Tetsuya Yamada, Tomoko Suzuki, Keiichi Shimizu and Kazuo Ichimura

National Institute of Floricultural Science, National Agriculture and Food Research Organization, Tsukuba 305–8519, Japan (K. Shibuya, K.I.); Tokyo University of Agriculture and Technology, Tokyo 183–8509, Japan (T.Y., T.S.); and Faculty of Agriculture, Kagoshima University, Kagoshima 890–0065, Japan (K. Shimizu)

The onset and progression of petal senescence, which is a type of programmed cell death (PCD), are highly regulated. Genes showing changes in expression during petal senescence in Japanese morning glory (Ipomoea nil) were isolated and examined to elucidate their function in PCD. We show here that a putative membrane protein, InPSR26, regulates progression of PCD during petal senescence in Japanese morning glory. InPSR26 is dominantly expressed in petal limbs and its transcript level increases prior to visible senescence symptoms. Transgenic plants with reduced InPSR26 expression (PSR26r lines) showed accelerated petal wilting, with PCD symptoms including cell collapse, ion and anthocyanin leakage, and DNA degradation accelerated in petals compared to wild-type plants. Transcript levels of autophagy- and PCD-related genes (InATG4, InATG8, InVPE, and InBI-1) were reduced in the petals of PSR26r plants. Autophagy visualized by monodansylcadaverine staining confirmed that autophagy is induced in senescing petal cells of wild-type plants and that the percentage of cells containing monodansylcadaverine-stained structures, most likely autophagosomes, was significantly lower in the petals of PSR26r plants, indicating reduced autophagic activity in the PSR26r plants. These results suggest that InPSR26 acts to delay the progression of PCD during petal senescence, possibly through regulation of the autophagic process. Our data also suggest that autophagy delays PCD in petal senescence.


1 This work was supported by grants from the National Agriculture and Food Research Organization, Japan (to K.S. and K.I.), and by Grants-in-Aid for Scientific Research from Ministry of Education, Culture, Sports, Science and Technology, Japan (grant nos. 18880009 and 19780019 to T.Y.).

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Kenichi Shibuya (shibuken{at}affrc.go.jp).

[W] The online version of this article contains Web-only data.

[OA] Open access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.108.127415

* Corresponding author; e-mail shibuken{at}affrc.go.jp.

Received August 1, 2008; accepted November 22, 2008; published November 26, 2008.







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