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Summary  Elongation of the Arabidopsis hypocotyl pushes the shoot‐producing meristem out of the soil by rapid expansion of cells already present in the embryo. This elongation process is shown here to be impaired by as much as 35% in mutants lacking  ABCB 19, an  ATP ‐binding cassette membrane protein required for polar auxin transport, during a limited time of fast growth in dim white light beginning 2.5 days after germination. The discovery of high ectopic expression of a cyclin B1;1‐based reporter of mitosis throughout  abcb19  hypocotyls without an equivalent effect on mitosis prompted investigations of the endoreplication variant of the cell cycle. Flow cytometry performed on nuclei isolated from upper (growing) regions of 3‐day‐old hypocotyls showed ploidy levels to be lower in  abcb19  mutants compared with wild type.   CCS 52A2  messenger  RNA  encoding a nuclear protein that promotes a shift from mitosis to endoreplication was lower in  abcb19  hypocotyls, and fluorescence microscopy showed the  CCS 52A2 protein to be lower in the nuclei of  abcb19  hypocotyls compared with wild type. Providing  abcb19  seedlings with nanomolar auxin rescued their low  CCS 52A2 levels, endocycle defects, aberrant cyclin B1;1 expression, and growth rate defect. The  abcb19 ‐like growth rate of  ccs52a2  mutants was not rescued by auxin, placing  CCS 52A2 after  ABCB 19‐dependent polar auxin transport in a pathway responsible for a component of ploidy‐related hypocotyl growth. A  ccs52A2  mutation did not affect the level or pattern of cyclin B1;1 expression, indicating that  CCS 52A2 does not mediate the effect of auxin on cyclin B1;1.

ABCB 19‐mediated polar auxin transport modulates Arabidopsis hypocotyl elongation and the endoreplication variant of the cell cycle