RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack

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Standard

RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack. / Liu, Jun; Elmore, James M.; Fuglsang, Anja Thoe; Palmgren, Michael; Staskawicz, Brian J.; Coaker, Gitta.

I: PLoS - Biology, Bind 7, Nr. 6, 2009.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Liu, J, Elmore, JM, Fuglsang, AT, Palmgren, M, Staskawicz, BJ & Coaker, G 2009, 'RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack', PLoS - Biology, bind 7, nr. 6. https://doi.org/10.1371/journal.pbio.1000139

APA

Liu, J., Elmore, J. M., Fuglsang, A. T., Palmgren, M., Staskawicz, B. J., & Coaker, G. (2009). RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack. PLoS - Biology, 7(6). https://doi.org/10.1371/journal.pbio.1000139

Vancouver

Liu J, Elmore JM, Fuglsang AT, Palmgren M, Staskawicz BJ, Coaker G. RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack. PLoS - Biology. 2009;7(6). https://doi.org/10.1371/journal.pbio.1000139

Author

Liu, Jun ; Elmore, James M. ; Fuglsang, Anja Thoe ; Palmgren, Michael ; Staskawicz, Brian J. ; Coaker, Gitta. / RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack. I: PLoS - Biology. 2009 ; Bind 7, Nr. 6.

Bibtex

@article{2e5cf1d0d2aa11dea1f3000ea68e967b,
title = "RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack",
abstract = "AbstractPathogen perception by the plant innate immune system is of central importance to plant survival and productivity. TheArabidopsis protein RIN4 is a negative regulator of plant immunity. In order to identify additional proteins involved in RIN4-mediated immune signal transduction, we purified components of the RIN4 protein complex. We identified six novelproteins that had not previously been implicated in RIN4 signaling, including the plasma membrane (PM) H+-ATPases AHA1and/or AHA2. RIN4 interacts with AHA1 and AHA2 both in vitro and in vivo. RIN4 overexpression and knockout lines exhibitdifferential PM H+-ATPase activity. PM H+-ATPase activation induces stomatal opening, enabling bacteria to gain entry intothe plant leaf; inactivation induces stomatal closure thus restricting bacterial invasion. The rin4 knockout line exhibitedreduced PM H+-ATPase activity and, importantly, its stomata could not be re-opened by virulent Pseudomonas syringae. Wealso demonstrate that RIN4 is expressed in guard cells, highlighting the importance of this cell type in innate immunity.These results indicate that the Arabidopsis protein RIN4 functions with the PM H+-ATPase to regulate stomatal apertures,inhibiting the entry of bacterial pathogens into the plant leaf during infection.",
author = "Jun Liu and Elmore, {James M.} and Fuglsang, {Anja Thoe} and Michael Palmgren and Staskawicz, {Brian J.} and Gitta Coaker",
note = "Paper id:: e1000139",
year = "2009",
doi = "10.1371/journal.pbio.1000139",
language = "English",
volume = "7",
journal = "P L o S Biology",
issn = "1544-9173",
publisher = "Public Library of Science",
number = "6",

}

RIS

TY - JOUR

T1 - RIN4 functions with plasma membrane H+-ATPases to regulate stomatal apertures during pathogen attack

AU - Liu, Jun

AU - Elmore, James M.

AU - Fuglsang, Anja Thoe

AU - Palmgren, Michael

AU - Staskawicz, Brian J.

AU - Coaker, Gitta

N1 - Paper id:: e1000139

PY - 2009

Y1 - 2009

N2 - AbstractPathogen perception by the plant innate immune system is of central importance to plant survival and productivity. TheArabidopsis protein RIN4 is a negative regulator of plant immunity. In order to identify additional proteins involved in RIN4-mediated immune signal transduction, we purified components of the RIN4 protein complex. We identified six novelproteins that had not previously been implicated in RIN4 signaling, including the plasma membrane (PM) H+-ATPases AHA1and/or AHA2. RIN4 interacts with AHA1 and AHA2 both in vitro and in vivo. RIN4 overexpression and knockout lines exhibitdifferential PM H+-ATPase activity. PM H+-ATPase activation induces stomatal opening, enabling bacteria to gain entry intothe plant leaf; inactivation induces stomatal closure thus restricting bacterial invasion. The rin4 knockout line exhibitedreduced PM H+-ATPase activity and, importantly, its stomata could not be re-opened by virulent Pseudomonas syringae. Wealso demonstrate that RIN4 is expressed in guard cells, highlighting the importance of this cell type in innate immunity.These results indicate that the Arabidopsis protein RIN4 functions with the PM H+-ATPase to regulate stomatal apertures,inhibiting the entry of bacterial pathogens into the plant leaf during infection.

AB - AbstractPathogen perception by the plant innate immune system is of central importance to plant survival and productivity. TheArabidopsis protein RIN4 is a negative regulator of plant immunity. In order to identify additional proteins involved in RIN4-mediated immune signal transduction, we purified components of the RIN4 protein complex. We identified six novelproteins that had not previously been implicated in RIN4 signaling, including the plasma membrane (PM) H+-ATPases AHA1and/or AHA2. RIN4 interacts with AHA1 and AHA2 both in vitro and in vivo. RIN4 overexpression and knockout lines exhibitdifferential PM H+-ATPase activity. PM H+-ATPase activation induces stomatal opening, enabling bacteria to gain entry intothe plant leaf; inactivation induces stomatal closure thus restricting bacterial invasion. The rin4 knockout line exhibitedreduced PM H+-ATPase activity and, importantly, its stomata could not be re-opened by virulent Pseudomonas syringae. Wealso demonstrate that RIN4 is expressed in guard cells, highlighting the importance of this cell type in innate immunity.These results indicate that the Arabidopsis protein RIN4 functions with the PM H+-ATPase to regulate stomatal apertures,inhibiting the entry of bacterial pathogens into the plant leaf during infection.

U2 - 10.1371/journal.pbio.1000139

DO - 10.1371/journal.pbio.1000139

M3 - Journal article

VL - 7

JO - P L o S Biology

JF - P L o S Biology

SN - 1544-9173

IS - 6

ER -

ID: 15864863