An enigma in the genetic responses of plants to salt stresses

Soil salinity is one of the main factors restricting crop production throughout the world. Various salt tolerance traits and the genes controlling these traits are responsible for coping with salinity stress in plants. These coping mechanisms include osmotic tolerance, ion exclusion, and tissue tolerance. Plants exposed to salinity stress sense the stress conditions, convey specific stimuli signals, and initiate responses against stress through the activation of tolerance mechanisms that include multiple genes and pathways. Advances in our understanding of the genetic responses of plants to salinity and their connections with yield improvement are essential for attaining sustainable agriculture. Although a wide range of studies have been conducted that demonstrate genetic variations in response to salinity stress, numerous questions need to be answered to fully understand plant tolerance to salt stress. This chapter provides an overview of previous studies on the genetic control of salinity stress in plants, including signaling, tolerance mechanisms, and the genes, pathways, and epigenetic regulators necessary for plant salinity tolerance

The STT3a Subunit Isoform of the Arabidopsis Oligosaccharyltransferase Controls Adaptive Responses to Salt/Osmotic Stress

Arabidopsis stt3a-1 and stt3a-2 mutations cause NaCl/osmotic sensitivity that is characterized by reduced cell division in the root meristem. Sequence comparison of the STT3a gene identified a yeast ortholog, STT3, which encodes an essential subunit of the oligosaccharyltransferase complex that is involved in protein N-glycosylation. NaCl induces the unfolded protein response in the endoplasmic reticulum (ER) and cell cycle arrest in root tip cells of stt3a seedlings, as determined by expression profiling of ER stress–responsive chaperone (BiP-GUS) and cell division (CycB1;1-GUS) genes, respectively. Together, these results indicate that plant salt stress adaptation involves ER stress signal regulation of cell cycle progression. Interestingly, a mutation (stt3b-1) in another Arabidopsis STT3 isogene (STT3b) does not cause NaCl sensitivity. However, the stt3a-1 stt3b-1 double mutation is gametophytic lethal. Apparently, STT3a and STT3b have overlapping and essential functions in plant growth and developmental processes, but the pivotal and specific protein glycosylation that is a necessary for recovery from the unfolded protein response and for cell cycle progression during salt/osmotic stress recovery is associated uniquely with the function of the STT3a isoform

SARS-CoV-2 neutralising antibody testing in Europe: towards harmonisation of neutralising antibody titres for better use of convalescent plasma and comparability of trial data.

We compared the performance of SARS-CoV-2 neutralising antibody testing between 12 European laboratories involved in convalescent plasma trials. Raw titres differed almost 100-fold differences between laboratories when blind-testing 15 plasma samples. Calibration of titres in relation to the reference reagent and standard curve obtained by testing a dilution series reduced the inter-laboratory variability ca 10-fold. The harmonisation of neutralising antibody quantification is a vital step towards determining the protective and therapeutic levels of neutralising&nbsp;antibodies.</p