alexa AtMKK1 mediates ABA-induced CAT1 expression and H2O2 production via AtMPK6-coupled signaling in Arabidopsis.


Enzyme Engineering

Author(s): Xing Y, Jia W, Zhang J

Abstract Share this page

Abstract Catalase controls cellular H(2)O(2) and plays important roles in the adaptation of plants to various stresses, but little is known about the signaling events that lead to the expression of CAT1 and the production of H(2)O(2). Here we report the dependence of CAT1 expression and H(2)O(2) production on a mitogen-activated protein kinase (MAPK) cascade. CAT1 transcript was induced in an ABA-dependent way and the induction was abolished in the T-DNA insertion mutant mkk1 (SALK_015914), while AtMKK1 overexpression significantly enhanced the ABA-induced CAT1 expression and H(2)O(2) production. AtMPK6, another component in the MAPK cascade, was also involved: mpk6 mutant blocked and overexpressing AtMPK6 enhanced the ABA-dependent expression of CAT1 and H(2)O(2) production. The activity of AtMPK6 was increased by ABA in an AtMKK1-dependent manner. These data clearly suggest an ABA-dependent signaling pathway connecting CAT1 expression through a phosphorelay including AtMKK1 and AtMPK6. In further support of this view, mkk1 mutant reduced both the sensitivity to ABA during germination and the drought tolerance of seedlings, whereas the AtMKK1 overexpression line showed the opposite responses when compared with the wild type. The data suggest AtMKK1-AtMPK6 to be a key module in an ABA-dependent signaling cascade causing H(2)O(2) production and stress responses. This article was published in Plant J and referenced in Enzyme Engineering

Relevant Expert PPTs

Relevant Speaker PPTs

Recommended Conferences

  • 3rd International Conference on Genetic and Protein Engineering
    Nov 02-Nov 03, 2017 Las Vegas, USA

Relevant Topics

Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version