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The molecular basis of cold acclimation in model plant Arabidopsis thaliana has been studied extensively. Transcriptional reprogramming occurs during cold acclimation to induce cold-regulated (COR) genes, responsible for producing cryoprotective molecules. Central to this transcriptional regulation are the CBF (C-repeat-binding factor) genes that encode AP2/ERF family transcription factors. There are several mechanisms by which the chloroplast may influence nuclear gene expression, a process known as retrograde signaling. Current model of retrograde signaling from plastid to nucleus includes GUN-dependent, ROS-dependent, and redox-dependent pathways. We have studied the effect of mutation in gene encoding GUN5, unrelated chloroplast protein involved in retrograde signaling, as well as mutations in the RpoTp, RpoTmp genes (nuclear-encoded chloroplast RNA-polymerase and nuclear-encoded chloroplast and mitochondria RNA-polymerase) and cpRNP genes (CP29A and CP31A), which are required to guarantee transcript stability of numerous chloroplast mRNAs. These mutations cause cold sensitivity. However, the expression of CBF genes is much higher than in WT, both basal level and cold-induced. Surprisingly, the expression of COR15a and COR47 does not change during the cold treatment and stay on the low level in mutant plants. Our results show, that cold response gene expression is controlled not only by environmental signals but also by intracellular signals from the chloroplasts. The chloroplast seems to be the target of cold acclimation processes, as the cold response system regulates gene expression of some chloroplast proteins (CORs). We provide evidence for the involvement of chloroplast RNA metabolism state and retrograde signals in the regulation of CBF cold response pathway.