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Enhanced gravi- and phototropism in plant mdr mutants mislocalizing the auxin efflux protein PIN1

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  • Bosl Noh

    (University of Wisconsin)

  • Anindita Bandyopadhyay

    (Purdue University)

  • Wendy Ann Peer

    (Purdue University)

  • Edgar P. Spalding

    (University of Wisconsin)

  • Angus S. Murphy

    (Purdue University)

Abstract

Many aspects of plant growth and development are dependent on the flow of the hormone auxin down the plant from the growing shoot tip where it is synthesized1,2. The direction of auxin transport in stems is believed to result from the basal localization within cells of the PIN1 membrane protein, which controls the efflux of the auxin anion3. Mutations in two genes homologous to those encoding the P-glycoprotein ABC transporters that are especially abundant in multidrug-resistant tumour cells in animals4 were recently shown to block polar auxin transport in the hypocotyls of Arabidopsis seedlings5. Here we show that the mdr mutants display faster and greater gravitropism and enhanced phototropism instead of the impaired curvature development expected in mutants lacking polar auxin transport. We find that these phenotypes result from a disruption of the normal accumulation of PIN1 protein along the basal end of hypocotyl cells associated with basipetal auxin flow. Lateral auxin conductance becomes relatively larger as a result, enhancing the growth differentials responsible for tropic responses.

Suggested Citation

  • Bosl Noh & Anindita Bandyopadhyay & Wendy Ann Peer & Edgar P. Spalding & Angus S. Murphy, 2003. "Enhanced gravi- and phototropism in plant mdr mutants mislocalizing the auxin efflux protein PIN1," Nature, Nature, vol. 423(6943), pages 999-1002, June.
  • Handle: RePEc:nat:nature:v:423:y:2003:i:6943:d:10.1038_nature01716
    DOI: 10.1038/nature01716
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    Cited by:

    1. Li, Yehua & Qiu, Yumou & Xu, Yuhang, 2022. "From multivariate to functional data analysis: Fundamentals, recent developments, and emerging areas," Journal of Multivariate Analysis, Elsevier, vol. 188(C).

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