RETINOBLASTOMA‐RELATED Has Both Canonical and Noncanonical Regulatory Functions During Thermo‐Morphogenic Responses in Arabidopsis Seedlings

ABSTRACT Warm temperatures accelerate plant growth, but the underlying molecular mechanism is not fully understood. Here, we show that increasing the temperature from 22°C to 28°C rapidly activates proliferation in the apical shoot and root meristems of wild‐type Arabidopsis seedlings. We found that one of the central regulators of cell proliferation, the cell cycle inhibitor RETINOBLASTOMA‐RELATED (RBR), is suppressed by warm temperatures. RBR became hyper‐phosphorylated at a conserved CYCLIN‐DEPENDENT KINASE (CDK) site in young seedlings growing at 28°C, in parallel with the stimulation of the expressions of the regulatory CYCLIN D/A subunits of CDK(s). Interestingly, while under warm temperatures ectopic RBR slowed down the acceleration of cell proliferation, it triggered elongation growth of post‐mitotic cells in the hypocotyl. In agreement, the central regulatory genes of thermomorphogenic response, including PIF4 and PIF7, as well as their downstream auxin biosynthetic YUCCA genes (YUC1‐2 and YUC8‐9) were all up‐regulated in the ectopic RBR expressing line but down‐regulated in a mutant line with reduced RBR level. We suggest that RBR has both canonical and non‐canonical functions under warm temperatures to control proliferative and elongation growth, respectively. Summary statement We discovered that warm temperatures activate cell proliferation in shoot and root apices by counteracting the canonical cell cycle inhibitor function of the RETINOBLASTOMA‐RELATED protein. Additionally, RBR was found to stimulate elongation of post‐mitotic hypocotyl cells in thermomorphogenesis.