In contrast to the accessory role of kinases in the modulation of auxin responses, several kinases have been found to have a direct involvement in the control of polar auxin transport. For example, Dai and co-workers (Dai et al. 2006) provided evidence that PAT is regulated by a MAPK cascade, as both loss-of-function and overexpression of the MAPKK BUD1/MKK7 resulted in phenotypes that suggest a role of MKK7 as a negative regulator of PAT (Dai et al. 2006). Moreover, the first and to date only identified PIN polarity determinant is the protein serine/threonine kinase PINOID (PID), as above-threshold activity of this kinase induces PIN sub-cellular re-targeting from the basal (root tip-facing) to the apical (shoot apex-facing) cell pole (Friml et al. 2004). PID was identified as a primary auxin-response gene (Benjamins et al. 2001), and therefore the kinase is likely to be part of a feedback loop by which auxin regulates the direction of its own transport in accordance with the canalization hypothesis, which describes the self-organizing role of auxin transport in tissue patterning (Sachs 1991). Below we will further elaborate on the role of PID, how its activity is regulated, and whether closely related protein kinases are involved in the polar targeting of the PIN auxin efflux carriers.
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