The bHLH transcription factor CgbHLH001 is a potential interaction partner of CDPK in halophyte Chenopodium glaucum

Abstract

Plants have evolved different abilities to adapt to the ever-fluctuating environments for sessility. Calcium-dependent protein kinase (CDPK) is believed to play a pivotal role in abiotic stress signaling. So far, study on the specific substrates that CDPK recognized in response to adversity is limited. In the present study, we revealed a potential interaction between CDPK and a bHLH transcription factor under salt stress in Chenopodium glaucum. First, we identified a CgCDPK, which was up-regulated under salt and drought stress; then by Y2H screening, CgCDPK was detected to be involved in interaction with a bHLH TF (named as CgbHLH001), which also positively respond to salt and drought stress. Further computational prediction and experiments including GST-pulldown and BiFC assays revealed that potential interaction existed between CgCDPK and CgbHLH001, and they might interact on the plasma membrane. In addition, CgCDPK-overexpressed transgenic tobacco line could significantly accumulate transcripts of NtbHLH (a homolog of CgbHLH001 in N. tabacum), which provided another evidence of correlation between CgCDPK and CgbHLH001. Our results suggest that CgbHLH001 can interact with CgCDPK in signal transduction pathway in response to abiotic stress, which should provide new evidence for further understanding of the substrate specificity of plant CDPK signaling pathway.

Revisiting the Role of Plant Transcription Factors in the Battle against Abiotic Stress

“…Using yeast two hybridization and CoIP approaches, recently, Zhou et al [ 222 ] screened out a small ubiquitin-like modifier E3 ligase MdSIZ1 as an interacting protein of MdMYB1 that enhances anthocyanin accumulation in apple under low temperature via sumoylation of MdMYB1 protein. Using both GST-pulldown and BiFC assays, Wang et al [ 223 ] disclosed that CgbHLH001 from Chenopodium glaucum is a potential interaction component of CgCDPK protein in the signal transduction pathway in response to drought or salt stress. In Arabidopsis, the interaction of WRKY8, a positive regulator of salt stress, with VQ9 (a VQ motif-containing protein) in the nucleus, decreases the DNA-binding activity of WRKY8, resulting in modulation of salt stress tolerance [ 224 ].…”

RNA-Seq analysis of Clerodendrum inerme (L.) roots in response to salt stress

“…The salt tolerance of a halophyte is determined by effective coordination between various physiological processes, metabolic pathways and gene networks under salt stress, including activation of antioxidant enzymes, induction and modulation of plant hormones, biosynthesis of compatible solutes and osmoprotectants, selective accumulation, exclusion of ions, and other mechanisms [15][16][17][18]. Furthermore, numerous genes that were isolated from halophytes have also been exploited by various modern biotechnological techniques to identify the genes that function in salt tolerance, including genes encoding for transcription factors [19,20], the Na + /H + antiporter gene [21,22] and genes encoding antioxidant enzymes [23,24]. The existence of these genes enhances the tolerance of plants to salt and provides more choices for the improvement of salt tolerance in crops.…”

Combinations of Small RNA, RNA, and Degradome Sequencing Uncovers the Expression Pattern of microRNA–mRNA Pairs Adapting to Drought Stress in Leaf and Root of Dactylis glomerata L.

“…The expression of genes involved in drought response change to maintain homeostasis of the cells [ 7 ]. For example, osmotic stress, a signal of drought stress, can activate genes in the mitogen-activated protein kinase (MAPK) and calcium-dependent protein kinase (CDPK) pathways, and promote or inhibit expression of downstream genes such as WRKY [ 8 ] and bHLH [ 9 ] transcription factors. MicroRNA (miRNA), an endogenous noncoding RNA that is about 22 nt [ 10 ], is a crucial post-transcriptional regulator that targets mRNAs to control mRNA degradation or repress the translation [ 11 ].…”