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.
Keyphrases
- transcription factor
- genome wide identification
- genome wide
- poor prognosis
- binding protein
- heat shock
- dna methylation
- gene expression
- arabidopsis thaliana
- protein protein
- amino acid
- genome wide analysis
- small molecule
- dna damage
- long non coding rna
- dna binding
- mass spectrometry
- oxidative stress
- climate change
- copy number