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A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling

Hybrids between Arabidopsis thaliana accessions are important in revealing the consequences of epistatic interactions in plants. F(1) hybrids between the A. thaliana accessions displaying either defense or developmental phenotypes have been revealing the roles of the underlying epistatic genes. The...

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Autores principales: Sageman-Furnas, Katelyn, Nurmi, Markus, Contag, Meike, Plötner, Björn, Alseekh, Saleh, Wiszniewski, Andrew, Fernie, Alisdair R, Smith, Lisa M, Laitinen, Roosa A E
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9282726/
https://www.ncbi.nlm.nih.gov/pubmed/35460255
http://dx.doi.org/10.1093/pcp/pcac056
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author Sageman-Furnas, Katelyn
Nurmi, Markus
Contag, Meike
Plötner, Björn
Alseekh, Saleh
Wiszniewski, Andrew
Fernie, Alisdair R
Smith, Lisa M
Laitinen, Roosa A E
author_facet Sageman-Furnas, Katelyn
Nurmi, Markus
Contag, Meike
Plötner, Björn
Alseekh, Saleh
Wiszniewski, Andrew
Fernie, Alisdair R
Smith, Lisa M
Laitinen, Roosa A E
author_sort Sageman-Furnas, Katelyn
collection PubMed
description Hybrids between Arabidopsis thaliana accessions are important in revealing the consequences of epistatic interactions in plants. F(1) hybrids between the A. thaliana accessions displaying either defense or developmental phenotypes have been revealing the roles of the underlying epistatic genes. The interaction of two naturally occurring alleles of the OUTGROWTH-ASSOCIATED KINASE (OAK) gene in Sha and Lag2-2, previously shown to cause a similar phenotype in a different allelic combination in A. thaliana, was required for the hybrid phenotype. Outgrowth formation in the hybrids was associated with reduced levels of salicylic acid, jasmonic acid and abscisic acid in petioles and the application of these hormones mitigated the formation of the outgrowths. Moreover, different abiotic stresses were found to mitigate the outgrowth phenotype. The involvement of stress and hormone signaling in outgrowth formation was supported by a global transcriptome analysis, which additionally revealed that TCP1, a transcription factor known to regulate leaf growth and symmetry, was downregulated in the outgrowth tissue. These results demonstrate that a combination of natural alleles of OAK regulates growth and development through the integration of hormone and stress signals and highlight the importance of natural variation as a resource to discover the function of gene variants that are not present in the most studied accessions of A. thaliana.
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spelling pubmed-92827262022-07-18 A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling Sageman-Furnas, Katelyn Nurmi, Markus Contag, Meike Plötner, Björn Alseekh, Saleh Wiszniewski, Andrew Fernie, Alisdair R Smith, Lisa M Laitinen, Roosa A E Plant Cell Physiol Regular Paper Hybrids between Arabidopsis thaliana accessions are important in revealing the consequences of epistatic interactions in plants. F(1) hybrids between the A. thaliana accessions displaying either defense or developmental phenotypes have been revealing the roles of the underlying epistatic genes. The interaction of two naturally occurring alleles of the OUTGROWTH-ASSOCIATED KINASE (OAK) gene in Sha and Lag2-2, previously shown to cause a similar phenotype in a different allelic combination in A. thaliana, was required for the hybrid phenotype. Outgrowth formation in the hybrids was associated with reduced levels of salicylic acid, jasmonic acid and abscisic acid in petioles and the application of these hormones mitigated the formation of the outgrowths. Moreover, different abiotic stresses were found to mitigate the outgrowth phenotype. The involvement of stress and hormone signaling in outgrowth formation was supported by a global transcriptome analysis, which additionally revealed that TCP1, a transcription factor known to regulate leaf growth and symmetry, was downregulated in the outgrowth tissue. These results demonstrate that a combination of natural alleles of OAK regulates growth and development through the integration of hormone and stress signals and highlight the importance of natural variation as a resource to discover the function of gene variants that are not present in the most studied accessions of A. thaliana. Oxford University Press 2022-04-23 /pmc/articles/PMC9282726/ /pubmed/35460255 http://dx.doi.org/10.1093/pcp/pcac056 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Regular Paper
Sageman-Furnas, Katelyn
Nurmi, Markus
Contag, Meike
Plötner, Björn
Alseekh, Saleh
Wiszniewski, Andrew
Fernie, Alisdair R
Smith, Lisa M
Laitinen, Roosa A E
A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling
title A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling
title_full A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling
title_fullStr A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling
title_full_unstemmed A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling
title_short A. thaliana Hybrids Develop Growth Abnormalities through Integration of Stress, Hormone and Growth Signaling
title_sort a. thaliana hybrids develop growth abnormalities through integration of stress, hormone and growth signaling
topic Regular Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9282726/
https://www.ncbi.nlm.nih.gov/pubmed/35460255
http://dx.doi.org/10.1093/pcp/pcac056
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