GSE196111
Co-expression networks of deacclimation-impaired mutants identified involvement of hypoxia and complex regulation of the cold stress release response
Plants adapt to cold, non-freezing temperatures through cold acclimation and subsequently lose the acquired freezing tolerance in warmer temperatures in a process called deacclimation. By measuring the freezing tolerance of mutant lines, this study identified that the loss of HRA1, LBD41, MBF1c and JUB1 slows the rate of deacclimation in the first four days in Arabidopsis thaliana. Comparative transcriptomic (RNA-Seq) and co-expression analysis of Col-0, mbf1c and jub1 during deacclimation identified an involvement of thermoswitches, cell wall remodeler and transporters in the regulation of the rate of deacclimation. In mbf1c and jub1 a unique increase in stress responsive genes and regulation of the jasmonic acid pathway was detected and linked to the mutants' retention of freezing tolerance during deacclimation. Hypoxia was observed to be induced in early deacclimation evidenced by an increase in ADH enzyme activity and upregulated gene expression of hypoxia markers (qRT-PCR). This work suggests that the overserved hypoxia response creates hypoxic niches within the plants and supports growth and development during deacclimation. Overall design: RNA-Sequencing of 28 d old Arabdiopsis thaliana plants of lines Col-0, mbf1c and jub1 at non-acclimated conditions (NonA), 3 days of cold acclimation (ACC), 2 days of deacclimation (Deacc2) and 4 days of deacclimation (Deacc4). For each condition and plant line three biological replicates where measured