Golgi anti-apoptotic proteins redundantly counteract cell death by inhibiting production of reactive oxygen species under endoplasmic reticulum stress.

Maintaining proteostasis in the endoplasmic reticulum (ER) is critical for cell viability and plant survival under adverse conditions. The unfolded protein response (UPR) pathways interact with reactive oxygen species (ROS) to precisely trigger adaptive outputs or cell death under ER stress with varying degrees. However, little information is known about the relationship between UPR signalling and ROS regulation. Here, Arabidopsis GOLGI ANTI-APOPTOTIC PROTEIN1 (GAAP1)-GAAP4 were found to play redundant positive roles under ER stress. Genetic analysis showed that GAAP4 played a role in INOSITOL-REQUIRING ENZYME (IRE1)-dependent and -independent pathways. In addition, GAAPs played negative roles to activate the adaptive UPR under conditions of stress. Quantitative biochemical analysis showed that mutations in GAAP genes decreased the oxidised glutathione content and altered the pattern of ROS and glutathione in early ER stress. When plants were challenged with unmitigated ER stress, mutations in GAAP advanced ROS accumulation, which was associated with a decline in adaptive UPR. These data indicated that GAAPs resist cell death by regulating glutathione content to inhibit ROS accumulation and maintain UPR during ER stress. They provide a basis for further analysis of the regulation of cell fate decision under ER stress.

RecQ helicase enhances homologous recombination in plants.

RecQ helicase is a key component in the RecF pathway of Escherichia coli for initiation of homologous recombination. Here, we demonstrate that transient expression of RecQ gene in rice embryogenic cell increases the homologous recombination efficiency as much as 4-fold. Further experiments reveal that this effect is influenced by the RecQ dosage. Stable expression of RecQ in rice dramatically increases the homologous recombination events 20- to 40-fold in leaf tissue from different transgenic lines. This is the first evidence indicating that overexpression of RecQ gene can stimulate homologous recombination in plants.

[Effect of methyl viologen on the Ca(2+)-ATPase activities of membrane vesicles in roots of rice seedlings].

The cold tolerance of rice (Oryza sativa L.) seedlings could be markedly improved by mild oxidative pretreatment (10 mumol/L methyl viologen (MV). The enhancement of chilling resistance induced by MV pretreatment could be inhibited by Ca(2+)-chelate ethyleneglycol-bis-(beta-aminoethylether) N,N-tetraacetic acid (EGTA, 10 mmol/L) and the calmodulin inhibitor chlorpromazine (CPZ, 0.5 mmol/L). The Ca(2+)-ATPase activity of root plasmolemma and tonoplast membrane as well as the Fe(CN)6(3-) reduction of plasmolemma were also enhanced by MV pretreatment. However, the above MV pretreatment effect could be inhibited by EGTA and CPZ, respectively. In vitro, Ca(2+)-ATPase activities in the two types of membrane vesicles were reduced by reactive oxygen species (H2O2, O2-., .OH). Results indicated that the enhancement of chilling resistance in rice seedlings with MV pretreatment was likely related to the effective activation of Ca(2+)-ATPase induced by calcium messenger of CaM, and the improved cold tolerance of the activities might be associated with the augmentation of cellular membrane protective ability caused by the MV pretreatment.