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ABCB 19‐mediated polar auxin transport modulates Arabidopsis hypocotyl elongation and the endoreplication variant of the cell cycle
Author(s) -
Wu Guosheng,
Carville Jacqueline S.,
Spalding Edgar P.
Publication year - 2016
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.13095
Subject(s) - endoreduplication , hypocotyl , biology , auxin , mitosis , microbiology and biotechnology , arabidopsis , polar auxin transport , meristem , ectopic expression , mutant , cell division , cell cycle , botany , biochemistry , cell , shoot , gene
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.