The amino acid region from 448-517 of CAMTA3 transcription factor containing a part of the TIG domain represses the N-terminal repression module function.

CAMTA3, a Ca ²⁺ -regulated transcription factor, is a repressor of plant immune responses. A truncated version of CAMTA3; CAMTA3 ³³⁴ called N-terminal repression module (NRM), and its extended version (CAMTA ⁴⁴⁷ ), which include the DNA binding domain, were previously reported to complement the camta3/2 mutant phenotype. Here, we generated a series of CAMTA3 truncated versions [the N-terminus (aa 1-517), C-terminus (aa 517-1032), R1 (aa 1-173), R2 (aa 174-345), R3 (aa 346-517), R4 (aa 517-689), R5 (aa 690-861) and R6 (aa 862-1032)], expressed in camta3 mutant and analyzed the phenotypes of the transgenic lines. Interestingly, unlike CAMTA ⁴⁴⁷ , extending the N-terminal region to 517 aa did not complement the camta3 phenotype, suggesting that the amino acid region from 448-517 (70 aa), which includes a part of the TIG domain suppresses the NRM activity. The C-terminus and other truncated versions (R1-R6) also failed to complement the camta3 mutant . Expressing the full length or NRM of CAMTA3 in camta3 plants suppressed the activation of immune-responsive genes and increased the expression of cold-induced genes. In contrast, the transgenic lines expressing the N- or C-terminus or R1-R6 of CAMTA3 showed expression patterns like those of the camta3 with enhanced expression of the defense genes and suppressed expression of the cold response genes. Furthermore, like camta3 , the transgenic lines expressing the N- or C-terminus, or R1-R6 of CAMTA3 exhibited higher levels of H ₂ O ₂ and increased resistance to a Pst DC3000 as compared to WT, NRM, or FL-CAMTA3 transgenic plants. Our studies identified a novel regulatory region in CAMTA3 that suppresses the NRM activity.
Supplementary Information: The online version contains supplementary material available at 10.1007/s12298-023-01401-w.
Competing Interests: Conflict of interestNo conflict of interest is declared by any of the authors.
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