A Haplotype-Specific Resistance Gene Regulated by BONZAI1 Mediates Temperature-Dependent Growth Control in Arabidopsis
Plant growth homeostasis and defense responses are regulated by BONZAI1 (BON1), an evolutionarily conserved gene. Here, we show that growth regulation by BON1 is mediated through defense responses. BON1 is a negative regulator of a haplotype-specific Resistance (R) gene SNC1. The bon1-1 loss-of-func...
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Published in | The Plant cell Vol. 16; no. 4; pp. 1060 - 1071 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
American Society of Plant Biologists
01.04.2004
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Subjects | |
Online Access | Get full text |
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Summary: | Plant growth homeostasis and defense responses are regulated by BONZAI1 (BON1), an evolutionarily conserved gene. Here, we show that growth regulation by BON1 is mediated through defense responses. BON1 is a negative regulator of a haplotype-specific Resistance (R) gene SNC1. The bon1-1 loss-of-function mutation activates SNC1, leading to constitutive defense responses and, consequently, reduced cell growth. In addition, a feedback amplification of the SNC1 gene involving salicylic acid is subject to temperature control, accounting for the regulation of growth and defense by temperature in bon1-1 and many other mutants. Thus, plant growth homeostasis involves the regulation of an R gene by BON1 and the intricate interplay between defense responses and temperature responses. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23 ObjectType-Feature-2 To whom correspondence should be addressed. E-mail jh299@cornell.edu; fax 607-255-5407. 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.plantcell.org) is: Jian Hua (jh299@cornell.edu). Article, publication date, and citation information can be found at www.plantcell.org/cgi/doi/10.1105/tpc.020479. These authors contributed equally to this paper. |
ISSN: | 1040-4651 1532-298X |
DOI: | 10.1105/tpc.020479 |