The shooty callus induced by suppression of tobacco CHRK1 receptor-like kinase is a phenocopy of the tobacco genetic tumor

J. H. Lee, D. M. Kim, Y. P. Lim, H. S. Pai

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

CHRK1 encodes a tobacco receptor-like kinase that contains a chitinase-like sequence in the extracellular domain. In a previous study, CHRK1-suppressed transgenic tobacco plants exhibited pleiotropic developmental abnormalities including spontaneous growth of shooty callus from emerging embryos in the absence of any exogenous hormones. In this study, we show that the CHRK1 shooty callus mimics tobacco genetic tumors in its morphology, physiology, and gene expression profiles. Similar to CHRK1 shooty callus, tobacco genetic tumors exhibit shooty callus morphology and hormone-independent shoot organogenesis. Both the CHRK1 callus and genetic tumors constitutively expressed KNOTTED1-type homeobox genes at the high levels, consistent with their vigorous shoot formation. These two types of calli exhibited cell death phenotypes, accompanied by high H2O2 production, increased ion leakage, and callose accumulation. Consistently, both types of calli constitutively expressed high levels of defense genes induced during pathogen-mediated HR cell death. These results, together with previous reports that both the CHRK1 shooty callus and tobacco genetic tumor contained high levels of cytokinin, indicate that CHRK1 shooty callus is a phenocopy of tobacco genetic tumor. CHRK1-mediated signal transduction may play a role in the formation of the genetic tumor in tobacco.

Original languageEnglish
Pages (from-to)397-403
Number of pages7
JournalPlant Cell Reports
Volume23
Issue number6
DOIs
Publication statusPublished - 2004 Nov 1

All Science Journal Classification (ASJC) codes

  • Agronomy and Crop Science
  • Plant Science

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