[No authors listed]
The growth of higher plants is under complex regulation to ensure the elaboration of developmental programmes under a changing environment. To dissect these regulatory circuits, we carried out genetic screens for Arabidopsis abnormal shoot (abs) mutants with altered shoot development. Here, we report the isolation of two dominant mutants, abs3-1D and abs4-1D, through activation tagging. Both mutants showed a 'bushy' loss of apical dominance phenotype. ABS3 and ABS4 code for two closely related putative Multidrug and Toxic Compound Extrusion (MATE) family of efflux transporters, respectively. ABS3 and ABS4, as well as two related MATE genes, ABS3-Like1 (ABS3L1) and ABS3L2, showed diverse tissue expression profiles but their gene products all localized to the late endosome/prevacuole (LE/PVC) compartment. The over-expression of these four genes individually led to the inhibition of hypocotyl cell elongation in the light. On the other hand, the quadruple knockout mutant (mateq) showed the opposite phenotype of an enhanced hypocotyl cell elongation in the light. Hypocotyl cell elongation and de-etiolation processes in the dark were also affected by the mutations of these genes. Exogenously applied sucrose attenuated the inhibition of hypocotyl elongation caused by abs3-1D and abs4-1D in the dark, and enhanced the hypocotyl elongation of mateq under prolonged dark treatment. We determined that ABS3 genetically interacts with the photoreceptor gene PHYTOCHROME B (PHYB). Our results demonstrate that ABS3 and related MATE family transporters are potential negative regulators of hypocotyl cell elongation and support a functional link between the endomembrane system, particularly the LE/PVC, and the regulation of plant cell elongation.
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