Methods and compositions to improve stress tolerance in plants include expression of a transcription factor that improves stress tolerance in plants.
Plants exhibit many physiological and biochemical changes when exposed to low temperature and during the process of cold acclimation, which in some plants, leads to the development of freezing tolerance. Survival of these tolerant plants at freezing temperatures depends on the modulation (upregulation or down-regulation) of specific sets of genes that are associated with the development of freezing tolerance.
The molecular mechanisms governing gene expression at low temperatures are not well understood. There is little information regarding the downstream signaling components leading to the transcriptional activation of specific sets of genes in response to low temperatures. Chilling and freezing temperatures affect the productivity and quality of plants including crop plants. Understanding of cold stress signaling has scientific and agricultural significance. Molecular and genetic studies have shown that many cold responsive genes are regulated through the CRT/DRE binding factor (CBF) family of transcriptional activators that bind the CRT/DRE promoter element (C-repeat/dehydration responsive element). Overexpression of CBF/DREB1 activates the transcription of some of the target genes and also increased tolerance of the transgenic plants to various stress responses.
After a period of low-temperature exposure, plants are able to better tolerate freezing temperatures (sustain less injury), a phenomenon referred to as cold acclimation. Part of the acclimation process involves the accumulation of gene transcripts via cold perception and signal transduction leading to promoter activation of target genes. One class of these target genes includes those encoding late-embryo abundant transcripts that contain in their promoters a C repeat (CRT)/dehydration responsive element (DRE). This element confers responsiveness to cold, desiccation, and salinity. The hormone abscisic acid (ABA) also can activate some genes responsive to cold that are in this class, such as the RD29A (COR78/LT178) gene. The RD29A gene contains both CRT/DRE and the ABA responsive element. Activation of RD29A can occur through the binding of transcription factors from the ethylene responsive element-binding protein/Apetala2 family. Specifically, the CRT/DRE-binding factor (CBF)1-4 transcription factors recognize the CRT/DRE and participate in adaptive (acclimating) responses to either cold (CBF1-3) or desiccation (CBF4). Ectopic overexpression of some CBF genes results in both activation of target genes and enhanced freezing, salt, or desiccation tolerance of transgenic plants. CBF transcription factor genes themselves are activated by stress, and a MYC-type transcription factor binds to and controls the activity of the CBF3 promoter in response to stress.
It is possible that other signal pathways in addition to those mediated by CBF transcription factors are also involved in stress-adaptive responses, including cold acclimation. For instance, the eskimo1 mutant is constitutively freezing tolerant and therefore does not require signaling through the cold-activated CBF factors. Also microarray transcript analysis experiments have shown that not all cold stress-responsive target genes contain CRT/DRE or are under the control of the CBF family. In addition, constitutive expression of the normally cold-induced CBF genes does not lead to full cold acclimation of Arabidopsis plants.
It is possible that other upstream signal components bypass CBF activators. Signal components that mediate cold tolerance and have little or no effect on CBF gene expression could act through such an alternative pathway or might modify CBF activity itself. Until now, no specific gene product has been to shown to act independently of CBF transcription in stress-mediated signaling response in plants.
Isolation and identification of genes that control cold or freezing tolerance by activating multiple genes are desired.