TCP transcription factors interact with ZED1-related kinases as components of the temperature-regulated immunity.

Abstract

The elevation of ambient temperature generally inhibits plant immunity, but the molecular regulations of immunity by ambient temperature in plants are largely elusive. We previously reported that the Arabidopsis HOPZ-ETI-DEFICIENT 1 (ZED1)-related kinases (ZRKs) mediate the temperature-sensitive immunity by inhibiting the transcription of SUPPRESSOR OF NPR1-1, CONSTITUTIVE 1 (SNC1). Here, we further demonstrate that the nucleus-localized ZED1 and ZRKs facilitate such inhibitory role in associating with the TEOSINTE BRANCHED1, CYCLOIDEA AND PROLIFERATING CELL FACTOR (TCP) transcription factors. We show that some of TCP members could physically interact with ZRKs and are induced by elevated temperature. Disruption of TCPs leads to a mild autoimmune phenotype, whereas overexpression of the TCP15 could suppress the autoimmunity activated by the overexpressed SNC1 in the snc1-2. These findings demonstrate that the TCP transcription factors associate with nuclear ZRK as components of the temperature-regulated immunity, which discloses a possible molecular mechanism underlying the regulation of immunity by ambient temperature in plants.