Increased Anion Channel Activity Is an Unavoidable Event in Ozone-Induced Programmed Cell Death

Ozone is a major secondary air pollutant often reaching high concentrations in urban areas under strong daylight, high temperature and stagnant high-pressure systems. Ozone in the troposphere is a pollutant that is harmful to the plant. generation by salicylic and abscisic acids. Anion channel activation was also shown to promote the accumulation of transcripts encoding vacuolar processing enzymes, a family of proteases previously reported to contribute to the disruption of vacuole integrity observed during programmed cell death.-induced programmed cell death. Because ion channels and more specifically anion channels assume a crucial position in cells, an understanding about the underlying role(s) for ion channels in the signalling pathway leading to programmed cell death is a subject that warrants future investigation

The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation

The formation of the mitotic spindle is a complex process that requires massive cellular reorganization. Regulation by mitotic kinases controls this entire process. One of these mitotic controllers is Aurora A kinase, which is itself highly regulated. In this study, we show that the nuclear pore protein ALADIN is a novel spatial regulator of Aurora A. Without ALADIN, Aurora A spreads from centrosomes onto spindle microtubules, which affects the distribution of a subset of microtubule regulators and slows spindle assembly and chromosome alignment. ALADIN interacts with inactive Aurora A and is recruited to the spindle pole after Aurora A inhibition. Of interest, mutations in ALADIN cause triple A syndrome. We find that some of the mitotic phenotypes that we observe after ALADIN depletion also occur in cells from triple A syndrome patients, which raises the possibility that mitotic errors may underlie part of the etiology of this syndrome

Aurora Kinases

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Type III effectors of E. amylovora: Synergistic and antagonistic effects

International audienceFunctional Type III secretion systems (TTSS) are required for pathogenicity of most gram-negative phytopathogenic bacteria including Ralstonia solanacearum, Erwinia amylovora, Pseudomonas syringae, Xanthomonas campestris, Pantoea stewartii, and Erwina herbicola pv. Gypsophilae. TTSS allows secretion into the medium and injection into the plant cell of bacterial proteins. Collectively, these bacterial proteins, called TTSS effectors, manipulate plant cell metabolism thereby playing a determinant role in disease initiation. Several effectors transiting through E. amylovora TTSS have been described. Among them, HrpN, HrpW and DspA/E are the focus of this review. Mutants affected in the biosynthesis of HrpN, HrpW or DspA/E is affected in their pathogenicity on host plants and their HR phenotype on non-host plants. HrpN and DspA/E act synergistically to trigger an oxidative stress on host plants. On the contrary, HrpN and HrpW act antagonistically on the triggering of cell death, HrpW being able to suppress HrpN induced cell death. Finally, DspA/E alone is able to trigger cell death on host and non-host plant, inhibiting at the same time some plant defense reactions. Therefore, these three effectors are important to modulate cell death and plant defense reactions on host and non-host plants

Type III effectors of E. amylovora: Synergistic and antagonistic effects

International audienceFunctional Type III secretion systems (TTSS) are required for pathogenicity of most gram-negative phytopathogenic bacteria including Ralstonia solanacearum, Erwinia amylovora, Pseudomonas syringae, Xanthomonas campestris, Pantoea stewartii, and Erwina herbicola pv. Gypsophilae. TTSS allows secretion into the medium and injection into the plant cell of bacterial proteins. Collectively, these bacterial proteins, called TTSS effectors, manipulate plant cell metabolism thereby playing a determinant role in disease initiation. Several effectors transiting through E. amylovora TTSS have been described. Among them, HrpN, HrpW and DspA/E are the focus of this review. Mutants affected in the biosynthesis of HrpN, HrpW or DspA/E is affected in their pathogenicity on host plants and their HR phenotype on non-host plants. HrpN and DspA/E act synergistically to trigger an oxidative stress on host plants. On the contrary, HrpN and HrpW act antagonistically on the triggering of cell death, HrpW being able to suppress HrpN induced cell death. Finally, DspA/E alone is able to trigger cell death on host and non-host plant, inhibiting at the same time some plant defense reactions. Therefore, these three effectors are important to modulate cell death and plant defense reactions on host and non-host plants

An early Ca2+ influx is a prerequisite to thaxtomin A-induced cell death in Arabidopsis thaliana cells

International audienceThe pathogenicity of various Streptomyces scabies isolates involved in potato scab disease was correlated with the production of thaxtomin A. Since calcium is known as an essential second messenger associated with pathogen-induced plant responses and cell death, it was investigated whether thaxtomin A could induce a Ca 2+ influx related to cell death and to other putative plant responses using Arabidopsis thaliana suspension cells, which is a convenient model to study plant–microbe interactions. A. thaliana cells were treated with micromolar concentrations of thaxto-min A. Cell death was quantified and ion flux variations were analysed from electrophysiological measurements with the apoaequorin Ca 2+ reporter protein and by external pH measurement. Involvement of anion and calcium channels in signal transduction leading to programmed cell death was determined by using specific inhibitors. These data suggest that this toxin induces a rapid Ca 2+ influx and cell death in A. thaliana cell suspensions. Moreover, these data provide strong evidence that the Ca 2+ influx induced by thaxtomin A is necessary to achieve this cell death and is a prerequisite to early thaxtomin A-induced responses: anion current increase, alkalization of the external medium, and the expression of PAL1 coding for a key enzyme of the phenylpropanoid pathway