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. In the present study, we show that lesion simulating disease 1 (LSD1) and enhanced disease susceptibility 1 (EDS1) are antagonistic regulators of UV-C-induced programmed cell death (PCD) in Arabidopsis thaliana. This regulatory dependence is manifested by a complex deregulation of photosynthesis, reactive oxygen species homeostasis, antioxidative enzyme activity and UV-responsive genes expression. We also prove that a UV-C radiation episode triggers apoptotic-like morphological changes within the mesophyll cells. Interestingly, chloroplasts are the first organelles that show features of UV-C-induced damage, which may indicate their primary role in PCD development. Moreover, we show that Arabidopsis Bax inhibitor 1 (AtBI1), which has been described as a negative regulator of plant PCD, is involved in LSD1-dependent cell death in response to UV-C. Our results imply that LSD1 and EDS1 regulate processes extinguishing excessive energy, reactive oxygen species formation and subsequent PCD in response to different stresses related to impaired electron transport.

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. Moreover, depending on growing conditions, it shows variations in water use efficiency, salicylic acid and hydrogen peroxide concentrations, photosystem II maximum efficiency, and transcription profiles. However, despite these changes, lsd1 demonstrates similar seed yield under all tested conditions. All of these traits depend on EDS1 and PAD4. The differences in the pathways prevailing in the lsd1 in various growing environments are manifested by the significantly smaller number of transcripts deregulated in the field compared with the laboratory, with only 43 commonly regulated genes. Our data indicate that LSD1, EDS1, and PAD4 participate in the regulation of various molecular and physiological processes that influence Arabidopsis fitness. On the basis of these results, we emphasize that the function of such important regulators as LSD1, EDS1, and PAD4 should be studied not only under stable laboratory conditions, but also in the environment abounding in multiple stresses.

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. Rapid changes in light intensity and quality often cause the absorption of energy, which is in excess of that required for photosynthesis. Such excessive light energy is considered to be a factor triggering photoinhibition and disturbance in ROS/hormonal homeostasis, which leads to cell death in foliar tissues. We highlight here the tight crosstalk between ROS- and SA-dependent pathways leading to light acclimation, and defence responses leading to pathogen resistance. We also show that LESION SIMULATING DISEASE 1 (LSD1) regulates and integrates these processes. Moreover, we discuss the role of plastid-nucleus signal transduction, photorespiration, photoelectrochemical signalling and 'light memory' in the regulation of acclimation and immune defence responses. All of these results suggest that plants have evolved a genetic system that simultaneously regulates systemic acquired resistance (SAR), cell death and systemic acquired acclimation (SAA).

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. In the present study we compared laboratory- and field-grown Arabidopsis thaliana plants in terms of photosynthetic efficiency in modulated light intensities and CO2 concentrations. We show here that the field-acclimated plants display highly efficient photosynthesis and are more tolerant to variable light intensities and CO2 concentrations than their laboratory-grown counterparts. We also demonstrate that some structural rearrangements of LHCII and PSII, together with altered pigments composition and stomatal density, are responsible for the differences in assimilation and photochemistry. Furthermore, we employ a transcript profiling approach to explain the genetic mechanisms underlying these adaptations and suggest that they are mainly induced by the high and fluctuating light intensities which occur in the natural environment.

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). We drew up denaturing high-performance liquid chromatography (DHPLC) conditions for analysis of intron 2 and exon 3 for two mutations (444+1G>A, I157T) and exon 10 for mutation 1100delC. We tested 251 patients and controls. Mutations show a similar frequency in the general population of Eastern Germany as in neighboring Poland (4.95% vs. 4.8% for the missense mutation I157T and 0.99% vs. 0.5% for the truncating mutations 444+1G>A and 1100delC). Investigation of these mutations by DHPLC is highly sensitive and less time-consuming compared to restriction fragment length polymorphism or allele-specific oligonucleotide polymerase chain reaction. It can be easily integrated into diagnostic testing.