Boron and blue light reduce responsiveness of Arabidopsis hypocotyls to exogenous auxins
We reported earlier that boron stimulates hypocotyl growth in several Arabidopsis ecotypes but not in the boron-deficient mutant bor1 - 1 . Others have shown that boron influences the metabolism and transport of the plant hormone auxin. We investigated how boron, in interaction with light, influence...
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Veröffentlicht in: | Plant growth regulation 2012-04, Vol.66 (3), p.293-301 |
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Zusammenfassung: | We reported earlier that boron stimulates hypocotyl growth in several
Arabidopsis
ecotypes but not in the boron-deficient mutant
bor1
-
1
. Others have shown that boron influences the metabolism and transport of the plant hormone auxin. We investigated how boron, in interaction with light, influences
Arabidopsis
hypocotyl growth responses to the exogenous auxins 1-NAA, 2,4-D and IAA. In either light condition, 1-NAA similarly inhibited hypocotyl growth in
bor1
-
1
and the corresponding WT (Col-0), while in both genotypes, boron did not essentially affect the extent of the inhibition. Whatever the light conditions and in the absence of boron, 2,4-D inhibited hypocotyl elongation in WT, while in BL seedlings, high responsiveness to 2,4-D vanished when boron was added to the culture medium. Hypocotyl of
bor1
-
1
seedlings in all boron concentrations tested and grown in the dark or RL responded to the auxin similar to WT plants. In BL, the mutant hypocotyls retained full sensitivity to 2,4-D at 0.1 mM H
3
BO
3
but lost that sensitivity by 2 mM. In both genotypes tested, in the dark or RL, IAA inhibited hypocotyl growth. Conversely, IAA stimulated hypocotyl elongation in both genotypes developed in BL at 0.1 mM H
3
BO
3
. That stimulation disappeared when the boron supply increased to 2 mM. Our results suggest that specifically in BL, boron reduces hypocotyl responsiveness to auxins 2,4-D or IAA via the functional transporter BOR1. Our results lead to a discussion of how BL and BOR1 influence the mechanisms of auxin transport into and out of the cell. |
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ISSN: | 0167-6903 1573-5087 |
DOI: | 10.1007/s10725-011-9646-2 |