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J Plant Physiol. 2011 Oct 15;168(15):1771-9. doi: 10.1016/j.jplph.2011.04.009.

Phytochrome interacting factors (PIFs) are essential regulators for sucrose-induced hypocotyl elongation in Arabidopsis.

Author information

1
Key Laboratory of Arid and Grassland Agroecology (Ministry of Education), School of Life Sciences, Lanzhou University, Lanzhou Gansu 730000, People's Republic of China.

Abstract

Phytochrome interacting factors (PIFs) are members of a subfamily of basic helix-loop-helix transcript factors and have been proposed to act as positive regulators of hypocotyl elongation under normal condition. Here, we show that PIF1, 3, 4, 5 together play a central role in sucrose-induced hypocotyl elongation. When seedlings grown in light were transferred to darkness, exogenously applied sucrose significantly induced hypocotyl elongation in wild type Col-0, but this effect was impaired in all tested pif mutants, especially in the quadruple mutant pif1pif3pif4pif5 (pifq). Subsequent experiments showed that under various light/dark (L/D) cycle conditions sucrose still markedly induced hypocotyl elongation in Col-0, but exhibited little effects in pifq. Phytohormone gibberellins (GAs) have been proven to be required for sucrose-induced hypocotyl elongation, but application of GA(3) (an active form of GAs) was not able to rescue the impairment observed in pifq, suggesting that impairment of sucrose-induced hypocotyl elongation in pifq is not due to the reduced endogenous GAs. Interestingly, through RT-PCR assay, we found that sucrose up-regulated the transcript level of PIF1, 3, 4, 5 in darkness. Furthermore, this effect was dependent on the presence of GAs. Additionally, under continuous light condition, sucrose markedly inhibited the hypocotyl elongation in Col-0 but not in pifq, whereas exogenous GA(3) could recover the repression in Col-0 but only showed slight effect in pifq. These results collectively indicate that PIFs together with GAs control the effect of sucrose on hypocotyl elongation in Arabidopsis seedlings.

PMID:
21684034
DOI:
10.1016/j.jplph.2011.04.009
[Indexed for MEDLINE]

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