Mapping quantitative trait loci for freezing tolerance in a recombinant inbred line population of Arabidopsis thaliana accessions Tenela and C24 reveals REVEILLE1 as negative regulator of cold acclimation.

The ability to increase freezing tolerance when exposed to low temperatures is a property of many plant species from temperate climates and involves a wide array of metabolic adjustments and changes in gene expression. In Arabidopsis thaliana, natural accessions show high variation in their acclimation capacity, and freezing tolerance correlates with natural habitat temperatures. To investigate the genetic basis of this variation, a recombinant inbred line population from reciprocal crosses between the accessions C24 and Tenela (Te), showing large variation in tolerance, was established.

A systems biology approach for the analysis of carbohydrate dynamics during acclimation to low temperature in Arabidopsis thaliana.

Low temperature is an important environmental factor affecting the performance and distribution of plants. During the so-called process of cold acclimation, many plants are able to develop low-temperature tolerance, associated with the reprogramming of a large part of their metabolism. In this study, we present a systems biology approach based on mathematical modelling to determine interactions between the reprogramming of central carbohydrate metabolism and the development of freezing tolerance in two accessions of Arabidopsis thaliana.

NONEXPRESSOR OF PATHOGENESIS-RELATED PROTEINS1 (NPR1) and some NPR1-related proteins are sensitive to salicylic acid.

NONEXPRESSOR OF PATHOGENESIS-RELATED PROTEINS1 (NPR1; also known as NIM1) is a master regulator of systemic acquired resistance (SAR). SAR is induced by salicylic acid (SA), leading to the expression of PATHOGENESIS-RELATED (PR) genes. Current evidence suggests that NPR1 is part of a transcription complex tethered to activation sequence-1 (as-1)-like cis-acting elements in PR-1 gene promoters through TGA transcription factors, and that SA-dependent PR-1 gene expression is regulated by NIM1-INTERACTING (NIMIN) proteins.