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Cited by 478

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Activation of a mitogen-activated protein kinase pathway is involved in disease resistance in tobacco

Open access
Yang, Kwang-Yeol, Liu, Yidong, Zhang, Shuqun·2001·Proceedings of the National Academy of Sciences

Abstract

Hypersensitive response (HR), a form of programmed cell death, is frequently associated with plant disease resistance. It has been proposed that mitogen-activated protein kinase (MAPK) cascades regulate HR cell death based on pharmacological studies by using kinase inhibitors. However, direct evidence is lacking. Here, we demonstrate that NtMEK2, a MAPK kinase, is upstream of salicylic acid-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK), two tobacco MAPKs that are activated by various pathogens or pathogen-derived elicitors. Expression of a constitutively active mutant of NtMEK2 induces HR-like cell death in tobacco, which is preceded by the activation of endogenous SIPK and WIPK. In addition, NtMEK2-SIPK/WIPK cascade appears to control the expression of 3-hydroxy-3-methylglutaryl CoA reductase ( HMGR ) and l -phenylalanine ammonia lyase ( PAL ), two defense genes encoding key enzymes in the phytoalexin and salicylic acid biosynthesis pathways. These results demonstrate that a plant MAPK cascade controls multiple defense responses against pathogen invasion.

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Metadata

Authors
Yang, K.-Y., Liu, Y., & Zhang, S.
Venue
Proceedings of the National Academy of Sciences
Published
2001-01-16
Volume
98
Issue
2
Pages
741-746
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2043161126
Cited by
478
References
1
FWCI
43.71
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Activation of a mitogen-activated protein kinase pathway is involved in disease resistance in tobacco. https://app.cochat.ai/papers/10.1073/pnas.98.2.741
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Yang, K.-Y., Liu, Y., & Zhang, S. (2001). Activation of a mitogen-activated protein kinase pathway is involved in disease resistance in tobacco. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.98.2.741

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