Circadian Clock-Regulated Phosphate Transporter PHT4;1 Plays an Important Role in Arabidopsis Defense

Wang, Guoying; Shi, Jiangli; Ng, Gina; Battle, Stephanie L.; Zhang, Chong; Lu, Hua

doi:10.1093/mp/ssr016

Cited by 78 publications

(71 citation statements)

References 74 publications

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“…7;Suárez-Ló pez et al, 2001) compared with Col-0. In addition, we recently showed that expression of NPR1 was not affected by the biological clock under our growth conditions (Wang et al, 2011a). Therefore, evidence from our studies did not support a role of the biological clock in regulating WIN3-and NPR1-mediated flowering time control.…”

Section: Win3 and Npr1 Act Additively In Regulating The Transition Tocontrasting

confidence: 74%

“…For instance, the component of the central oscillator of the Arabidopsis clock, CIRCADIAN CLOCK ASSOCIATED1, was recently shown to play a direct role in plant defense (Wang et al, 2011b). In addition, the expression of some defense genes is also known to be under the control of the biological clock (Wang et al, 2001(Wang et al, , 2011aSauerbrunn and Schlaich, 2004;Weyman et al, 2006). However, we did not detect any change in the expression of the circadian clockregulated gene CO in both win3 and npr1 mutants (Fig.…”

Section: Win3 and Npr1 Act Additively In Regulating The Transition Tomentioning

confidence: 58%

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Multiple Roles of WIN3 in Regulating Disease Resistance, Cell Death, and Flowering Time in Arabidopsis

et al. 2011

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The salicylic acid (SA) regulatory gene HOPW1-1-INTERACTING3 (WIN3) was previously shown to confer resistance to the biotrophic pathogen Pseudomonas syringae. Here, we report that WIN3 controls broad-spectrum disease resistance to the necrotrophic pathogen Botrytis cinerea and contributes to basal defense induced by flg22, a 22-amino acid peptide derived from the conserved region of bacterial flagellin proteins. Genetic analysis indicates that WIN3 acts additively with several known SA regulators, including PHYTOALEXIN DEFICIENT4, NONEXPRESSOR OF PR GENES1 (NPR1), and SA INDUCTION-DEFICIENT2, in regulating SA accumulation, cell death, and/or disease resistance in the Arabidopsis (Arabidopsis thaliana) mutant acd6-1. Interestingly, expression of WIN3 is also dependent on these SA regulators and can be activated by cell death, suggesting that WIN3-mediated signaling is interconnected with those derived from other SA regulators and cell death. Surprisingly, we found that WIN3 and NPR1 synergistically affect flowering time via influencing the expression of flowering regulatory genes FLOWERING LOCUS C and FLOWERING LOCUS T. Taken together, our data reveal that WIN3 represents a novel node in the SA signaling networks to regulate plant defense and flowering time. They also highlight that plant innate immunity and development are closely connected processes, precise regulation of which should be important for the fitness of plants.

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Section: Win3 and Npr1 Act Additively In Regulating The Transition Tocontrasting

confidence: 74%

Section: Win3 and Npr1 Act Additively In Regulating The Transition Tomentioning

confidence: 58%

Multiple Roles of WIN3 in Regulating Disease Resistance, Cell Death, and Flowering Time in Arabidopsis

et al. 2011

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“…Thus, the change of acd6-1 dwarfism induced by second-site mutations could be conveniently used as a visual readout to provide a rapid assessment of the effect of these second-site mutations in some genes on defense responses. acd6-1 has been successfully used in genetic analyses to reveal epistatic relationships between defense mutants and in a genetic screen to identify, to our knowledge, novel defense genes (Song et al, 2004;Lu et al, 2009;Ng et al, 2011;Wang et al, 2011aWang et al, , 2011bWang et al, , 2014a. We found that while acd6-1 sim-1 resembled acd6-1 in plant morphology, acd6-1 smr1-1 and acd6-1 sim-1 smr1-1 were significantly larger than acd6-1 plants (Fig.…”

Section: Smr1 Contributes To Sa-mediated Defensementioning

confidence: 77%

Differential Roles of Two Homologous Cyclin-Dependent Kinase Inhibitor Genes in Regulating Cell Cycle and Innate Immunity in Arabidopsis

et al. 2015

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Precise cell-cycle control is critical for plant development and responses to pathogen invasion. Two homologous cyclindependent kinase inhibitor genes, SIAMESE (SIM) and SIM-RELATED 1 (SMR1), were recently shown to regulate Arabidopsis (Arabidopsis thaliana) defense based on phenotypes conferred by a sim smr1 double mutant. However, whether these two genes play differential roles in cell-cycle and defense control is unknown. In this report, we show that while acting synergistically to promote endoreplication, SIM and SMR1 play different roles in affecting the ploidy of trichome and leaf cells, respectively. In addition, we found that the smr1-1 mutant, but not sim-1, was more susceptible to a virulent Pseudomonas syringae strain, and this susceptibility could be rescued by activating salicylic acid (SA)-mediated defense. Consistent with these results, smr1-1 partially suppressed the dwarfism, high SA levels, and cell death phenotypes in acd6-1, a mutant used to gauge the change of defense levels. Thus, SMR1 functions partly through SA in defense control. The differential roles of SIM and SMR1 are due to differences in temporal and spatial expression of these two genes in Arabidopsis tissues and in response to P. syringae infection. In addition, flow-cytometry analysis of plants with altered SA signaling revealed that SA is necessary, but not sufficient, to change cell-cycle progression. We further found that a mutant with three CYCD3 genes disrupted also compromised disease resistance to P. syringae. Together, this study reveals differential roles of two homologous cyclin-dependent kinase inhibitors in regulating cell-cycle progression and innate immunity in Arabidopsis and provides insights into the importance of cell-cycle control during host-pathogen interactions.

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“…We identified a lesion mimic mutant in the background of a transposon insertional mutant for the phosphate transporter gene PHT4;1 20. Positional cloning revealed that the lesion mimic phenotype was not associated with the pht4;1 mutation, but was due to a mutation in the FZL gene.…”

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confidence: 97%

A Role of the FUZZY ONIONS LIKE Gene in Regulating Cell Death and Defense in Arabidopsis

Tremblay

Seabolt

Zeng

et al. 2016

Sci Rep

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Programmed cell death (PCD) is critical for development and responses to environmental stimuli in many organisms. FUZZY ONIONS (FZO) proteins in yeast, flies, and mammals are known to affect mitochondrial fusion and function. Arabidopsis FZO-LIKE (FZL) was shown as a chloroplast protein that regulates chloroplast morphology and cell death. We cloned the FZL gene based on the lesion mimic phenotype conferred by an fzl mutation. Here we provide evidence to support that FZL has evolved new function different from its homologs from other organisms. We found that fzl mutants showed enhanced disease resistance to the bacterial pathogen Pseudomonas syringae and the oomycete pathogen Hyaloperonospora arabidopsidis. Besides altered chloroplast morphology and cell death, fzl showed the activation of reactive oxygen species (ROS) and autophagy pathways. FZL and the defense signaling molecule salicylic acid form a negative feedback loop in defense and cell death control. FZL did not complement the yeast strain lacking the FZO1 gene. Together these data suggest that the Arabidopsis FZL gene is a negative regulator of cell death and disease resistance, possibly through regulating ROS and autophagy pathways in the chloroplast.

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Circadian Clock-Regulated Phosphate Transporter PHT4;1 Plays an Important Role in Arabidopsis Defense

Cited by 78 publications

References 74 publications

Multiple Roles of WIN3 in Regulating Disease Resistance, Cell Death, and Flowering Time in Arabidopsis

Multiple Roles of WIN3 in Regulating Disease Resistance, Cell Death, and Flowering Time in Arabidopsis

Differential Roles of Two Homologous Cyclin-Dependent Kinase Inhibitor Genes in Regulating Cell Cycle and Innate Immunity in Arabidopsis

A Role of the FUZZY ONIONS LIKE Gene in Regulating Cell Death and Defense in Arabidopsis

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