Lesion simulating disease 1 and enhanced disease susceptibility 1 differentially regulate UV-C-induced photooxidative stress signalling and programmed cell death in Arabidopsis thaliana.

As obligate photoautotrophs, plants are inevitably exposed to ultraviolet (UV) radiation. Because of stratospheric ozone depletion, UV has become more and more dangerous to the biosphere. Therefore, it is important to understand UV perception and signal transduction in plants.

Lesion simulating disease1, enhanced disease susceptibility1, and phytoalexin deficient4 conditionally regulate cellular signaling homeostasis, photosynthesis, water use efficiency, and seed yield in Arabidopsis.

There is growing evidence that for a comprehensive insight into the function of plant genes, it is crucial to assess their functionalities under a wide range of conditions. In this study, we examined the role of lesion simulating disease1 (LSD1), enhanced disease susceptibility1 (EDS1), and phytoalexin deficient4 (PAD4) in the regulation of photosynthesis, water use efficiency, reactive oxygen species/hormonal homeostasis, and seed yield in Arabidopsis (Arabidopsis thaliana) grown in the laboratory and in the field. We demonstrate that the LSD1 null mutant (lsd1), which is known to exhibit a runaway cell death in nonpermissive conditions, proves to be more tolerant to combined drought and high-light stress than the wild type.

Multivariable environmental conditions promote photosynthetic adaptation potential in Arabidopsis thaliana.

Most of our knowledge on the regulation of photosynthesis originates from studies performed in highly controlled laboratory conditions. However, in their natural habitats plants are simultaneously subjected to a broad range of abiotic and biotic stimuli which influence photosynthetic efficiency; hence there is an emerging need to examine the process of photosynthesis under multivariable field conditions in order to elucidate the mechanisms that underlie its regulation. Such knowledge has potential for providing novel targets that would improve both crop yield and performance.

Light acclimation, retrograde signalling, cell death and immune defences in plants.

This review confronts the classical view of plant immune defence and light acclimation with recently published data. Earlier findings have linked plant immune defences to nucleotide-binding site leucine-rich repeat (NBS-LRR)-dependent recognition of pathogen effectors and to the role of plasma membrane-localized NADPH-dependent oxidoreductase (AtRbohD), reactive oxygen species (ROS) and salicylic acid (SA). However, recent results suggest that plant immune defence also depends on the absorption of excessive light energy and photorespiration.

A simple method of investigating mutations in CHEK2 by DHPLC: a study of the German populations of Saxony, Saxony-Anhalt, and Thuringia.

Allele variants of the CHEK2 gene have been found to be associated with several types of cancer, including cancer of the breast, prostate, lung, and ovary. In the Polish population, three founder mutations of CHEK2 have been identified: I157T, 444+1G>A (formerly IVS2+1G>A), and 1100delC. The aim of our study was to establish a simple method to identify founder CHEK2 mutations and determine the prevalence of these changes in the population of Eastern Germany (Saxony, Saxony-Anhalt, and Thuringia).