High impact information on CPC

• Analysis in combination with other root hair mutations showed that CPC may work together with the TTG gene and upstream of the GL2 gene [1].
• Thus, the CPC gene determines the fate of epidermal cell differentiation in Arabidopsis [1].
• The truncated MYB encoded by CPC mediates a lateral inhibition mechanism to negatively regulate WER, GL2, and its own gene in the alternative position (H) to induce the hair fate [2].
• Cell-to-cell movement of CPC is important for the differentiation of epidermal cells into trichoblasts (root hair cells) [3].
• Analyses with a secretion inhibitor, Brefeldin A, and with an rhd3 mutant defective in the secretion process in root epidermis suggested that intercellular CPC movement is mediated through plasmodesmata [3].

Biological context of CPC

• Deletion analyses of the CPC promoter revealed that hairless cell-specific transcription of the CPC gene required a 69 bp sequence, and a tandem repeat of this region was sufficient for its expression in epidermis [4].
• Positional cues bias the expression of the WER MYB gene, leading to the induction of CPC and GL2 in cells located in a particular position (N) and adoption of the nonhair fate [2].
• We show that WER, GL2 and CPC are expressed and active during the stages of embryogenesis when the pattern of cells in the epidermis of the root-hypocotyl axis forms [5].
• An ETC1 promoter-reporter gene fusion is expressed in the developing trichome and non-hair cells, similar to the expression of TRY and CPC [6].
• The etc1 single mutant has no significant phenotype, but it enhances the effect of cpc and try on trichome and root hair development, which shows that ETC1 function is partially redundant with TRY and CPC [6].

Anatomical context of CPC

• Furthermore, the fusion of CPC to tandem-GFPs defined the capability of CPC to increase the size exclusion limit of plasmodesmata [3].

Regulatory relationships of CPC

• Here, we show that CPC is also predominantly expressed in the hairless cells, but not in the neighboring hair-forming cells, and that CPC protein moves to the hair-forming cells and represses the GL2 expression [7].
• In addition, we used the glucocorticoid receptor (GR) inducible system to show that CPC transcription is regulated directly by WER [8].

Other interactions of CPC

• To evaluate the tissue-specificity of CPC movement, CPC:GFP was expressed in the stele using the SHR promoter and in trichoblasts using the EGL3 promoter [3].
• These results suggest that GL3/EGL3 accumulation in the N cells is dependent on specification of the hair cell fate, which itself is known to be influenced (via CPC-mediated lateral inhibition) by the non-hair cells [9].
• Binding between the WER protein and both WBSs (WBSI and WBSII), and the importance of the two WBSs in CPC promoter activity were confirmed in Arabidopsis [8].
• These results suggest that ETC1, TRY, and CPC act in concert to repress the trichome cell fate in the shoot epidermis and the non-hair cell fate in the root epidermis [6].
• The distinction between epidermal cells contacting one or two cortical cells was accounted for by fixing the initial states of CPC and ETR1 proteins [10].

Analytical, diagnostic and therapeutic context of CPC

• Furthermore, we show that these bHLH proteins require a functional WER MYB protein for their action, and they physically interact with WER and CPC in the yeast two-hybrid assay [11].

References