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

Journal Article (Journal Article)

Hybrids between Arabidopsis thaliana accessions are important in revealing the consequences of epistatic interactions in plants. F1 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.

Full Text

Duke Authors

Cited Authors

  • Sageman-Furnas, K; Nurmi, M; Contag, M; Plötner, B; Alseekh, S; Wiszniewski, A; Fernie, AR; Smith, LM; Laitinen, RAE

Published Date

  • July 2022

Published In

Volume / Issue

  • 63 / 7

Start / End Page

  • 944 - 954

PubMed ID

  • 35460255

Pubmed Central ID

  • PMC9282726

Electronic International Standard Serial Number (EISSN)

  • 1471-9053

International Standard Serial Number (ISSN)

  • 0032-0781

Digital Object Identifier (DOI)

  • 10.1093/pcp/pcac056

Language

  • eng