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The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants

During floral induction and flower development plants undergo delicate phase changes which are under tight molecular control. MADS-box transcription factors have been shown to play pivotal roles during these transition phases. SHORT VEGETATIVE PHASE (SVP) and AGAMOUS LIKE 24 (AGL24) are important re...

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Autores principales: Fornara, Fabio, Gregis, Veronica, Pelucchi, Nilla, Colombo, Lucia, Kater, Martin
Formato: Texto
Lenguaje:English
Publicado: Oxford University Press 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413287/
https://www.ncbi.nlm.nih.gov/pubmed/18453531
http://dx.doi.org/10.1093/jxb/ern083
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author Fornara, Fabio
Gregis, Veronica
Pelucchi, Nilla
Colombo, Lucia
Kater, Martin
author_facet Fornara, Fabio
Gregis, Veronica
Pelucchi, Nilla
Colombo, Lucia
Kater, Martin
author_sort Fornara, Fabio
collection PubMed
description During floral induction and flower development plants undergo delicate phase changes which are under tight molecular control. MADS-box transcription factors have been shown to play pivotal roles during these transition phases. SHORT VEGETATIVE PHASE (SVP) and AGAMOUS LIKE 24 (AGL24) are important regulators both during the transition to flowering and during flower development. During vegetative growth they exert opposite roles on floral transition, acting as repressor and promoter of flowering, respectively. Later during flower development they act redundantly as negative regulators of AG expression. In rice, the orthologues of SVP and AGL24 are OsMADS22, OsMADS47, and OsMADS55 and these three genes are involved in the negative regulation of brassinosteroid responses. In order to understand whether these rice genes have maintained the ability to function as regulators of flowering time in Arabidopsis, complementation tests were performed by expressing OsMADS22 and OsMADS47 in the svp and agl24 mutants. The results show that the rice genes are not able to complement the flowering-time phenotype of the Arabidopsis mutants, indicating that they are biologically inactive in Arabidopsis. Nevertheless, they cause floral reversions, which mimic the SVP and AGL24 floral overexpressor phenotypes. Yeast two-hybrid analysis suggests that these floral phenotypes are probably the consequence of protein interactions between OsMADS22 and OsMADS47 and other MADS-box proteins which interfere with the formation of complexes required for normal flower development.
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spelling pubmed-24132872009-02-25 The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants Fornara, Fabio Gregis, Veronica Pelucchi, Nilla Colombo, Lucia Kater, Martin J Exp Bot Research Papers During floral induction and flower development plants undergo delicate phase changes which are under tight molecular control. MADS-box transcription factors have been shown to play pivotal roles during these transition phases. SHORT VEGETATIVE PHASE (SVP) and AGAMOUS LIKE 24 (AGL24) are important regulators both during the transition to flowering and during flower development. During vegetative growth they exert opposite roles on floral transition, acting as repressor and promoter of flowering, respectively. Later during flower development they act redundantly as negative regulators of AG expression. In rice, the orthologues of SVP and AGL24 are OsMADS22, OsMADS47, and OsMADS55 and these three genes are involved in the negative regulation of brassinosteroid responses. In order to understand whether these rice genes have maintained the ability to function as regulators of flowering time in Arabidopsis, complementation tests were performed by expressing OsMADS22 and OsMADS47 in the svp and agl24 mutants. The results show that the rice genes are not able to complement the flowering-time phenotype of the Arabidopsis mutants, indicating that they are biologically inactive in Arabidopsis. Nevertheless, they cause floral reversions, which mimic the SVP and AGL24 floral overexpressor phenotypes. Yeast two-hybrid analysis suggests that these floral phenotypes are probably the consequence of protein interactions between OsMADS22 and OsMADS47 and other MADS-box proteins which interfere with the formation of complexes required for normal flower development. Oxford University Press 2008-05 2008-05-02 /pmc/articles/PMC2413287/ /pubmed/18453531 http://dx.doi.org/10.1093/jxb/ern083 Text en © 2008 The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. This paper is available online free of all access charges (see http://jxb.oxfordjournals.org/open_access.html for further details)
spellingShingle Research Papers
Fornara, Fabio
Gregis, Veronica
Pelucchi, Nilla
Colombo, Lucia
Kater, Martin
The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants
title The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants
title_full The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants
title_fullStr The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants
title_full_unstemmed The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants
title_short The rice StMADS11-like genes OsMADS22 and OsMADS47 cause floral reversions in Arabidopsis without complementing the svp and agl24 mutants
title_sort rice stmads11-like genes osmads22 and osmads47 cause floral reversions in arabidopsis without complementing the svp and agl24 mutants
topic Research Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2413287/
https://www.ncbi.nlm.nih.gov/pubmed/18453531
http://dx.doi.org/10.1093/jxb/ern083
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