Iwate University, Morioka, Japan
Plant growth and development is regulated by many factors including temperature stress. Low temperature significantly reduces the crop productivity world-wide. Previously we demonstrated that cold-induced inhibition of root growth is linked to the inhibition of the trafficking of a subset of auxin transport proteins that alters the cellular homeostasis of auxin. The cell cytoskeletal component, actin plays an important role in cellular trafficking by providing a track for the protein movement. The vegetative growth of Arabidopsis is largely controlled by three actin isovariants, ACT8, ACT2 and ACT7. However, the roles of these actin isovariants in cold response remain elusive. To better understand the role of actin in cold stress response, we screened the response of the single actin isovariant mutants to cold using root growth recovery assay after providing cold stress at 4? for 12h. The screening results revealed that loss of ACT8 but not ACT2 results in hypersensitive response to cold stress, although they belong to the same clade. The root growth recovery is severely delayed in act8-2 mutant, while act2-1 mutant shows wild-type response to cold stress. Compared with wild-type, cellular auxin homeostasis is drastically altered in act8-2 mutant root both after cold stress and during recovery stage as judged by the auxin marker line IAA2-GUS. The altered redistribution of auxin in act8-2 mutant under cold stress was found to be directly linked to the altered trafficking of PIN2 and AUX1 which serve as efflux and influx carriers of auxin respectively. In addition, a significant change was also observed in endoplasmic reticulum trafficking under cold stress. Consistently, in act8-2 mutant, endoplasmic reticulum trafficking was much reduced compared with wild-type under cold stress. Collectively, these results suggest that actin isovariant ACT8 specifically regulates the cold stress response in Arabidopsis root through modulating the trafficking of auxin transporter proteins and endoplasmic reticulum.