How plants maintain growth under nonfreezing low temperatures (chilling) is not well understood. Here we use hypocotyl elongation under dark to investigate the molecular mechanisms for chilling growth in Arabidopsis thaliana. The function of HsfA1d (Heat shock transcription factor A1d) in chilling growth is investigated by physiological and molecular characterization of its mutants. Subcellular localization of HsfA1d under chilling is analyzed. Potential target genes of HsfA1d were identified by transcriptome analysis, chromatin immunoprecipitation, transcriptional activation assay and mutant characterization. HsfA1d is a positive regulator of hypocotyl elongation under chilling. It promotes expression of a large number of ribosome biogenesis genes to a moderate but significant extent under chilling. HsfA1d could bind to the promoter regions of two ribosome protein genes tested and promote their expression. The loss-of-function of one ribosome gene also reduced hypocotyl elongation under chilling. In addition, HsfA1d did not have increased nuclear accumulation under chilling and its basal nuclear accumulation is promoted by a salicylic acid receptor under chilling. This study thus unveils a new HsfA1d-mediated pathway that promotes the expression of cytosolic and plastid cytosolic and plastid ribosomal protein genes which may maintain overall protein translation for plant growth in chilling.

Ammonium (NH) inhibits primary root (PR) growth in most plant species when present even at moderate concentrations. Previous studies have shown that transport of indole-3-acetic acid (IAA) is critical to maintaining root elongation under high-NH stress. However, the precise regulation of IAA homeostasis under high-NH stress (HAS) remains unclear. In this study, qRT-PCR, RNA-seq, free IAA and IAA conjugate and PR elongation measurements were conducted in genetic mutants to investigate the role of IAA biosynthesis and conjugation under HAS. Our data clearly show that HAS decreases free IAA in roots by increasing IAA inactivation but does not decrease IAA biosynthesis, and that the IAA-conjugating genes GH3.1, GH3.2, GH3.3, GH3.4, and GH3.6 function as the key genes in regulating high-NH sensitivity in the roots. Furthermore, the analysis of promoter::GUS staining in situ and genetic mutants reveals that HAS promotes IAA conjugation in the elongation zone (EZ), which may be responsible for the PR inhibition observed under HAS. This study provides potential new insight into the role of auxin in the improvement of tolerance to NH.