Compensatory mutations in predicted metal transporters modulate auxin conjugate responsiveness in Arabidopsis.

Compensatory mutations in predicted metal transporters modulate auxin conjugate responsiveness in Arabidopsis.
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DOI:
10.1534/g3.112.004655
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发表时间:
2013-01
期刊:
G3 (Bethesda, Md.)
影响因子:
--
通讯作者:
Bartel B
Bartel B
中科院分区:
其他
文献类型:
--
作者:
Rampey RA;Baldridge MT;Farrow DC;Bay SN;Bartel B

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Levels of the phytohormone indole-3-acetic acid (IAA) can be altered by the formation and hydrolysis of IAA conjugates. The isolation and characterization of Arabidopsis thaliana mutants with reduced IAA-conjugate sensitivity and wild-type IAA responses is advancing the understanding of auxin homeostasis by uncovering the factors needed for conjugate metabolism. For example, the discovery that the IAA-Ala-resistant mutant iar1 is defective in a protein in the ZIP family of metal transporters uncovered a link between metal homeostasis and IAA-conjugate sensitivity. To uncover additional factors impacting auxin conjugate metabolism, we conducted a genetic modifier screen and isolated extragenic mutations that restored IAA-amino acid conjugate sensitivity to the iar1 mutant. One of these suppressor mutants is defective in a putative cation diffusion facilitator, MTP5 (At3g12100; formerly known as MTPc2). Loss of MTP5 function restored IAA conjugate sensitivity to iar1 but not to mutants defective in IAA-amino acid conjugate amidohydrolases. Our results are consistent with a model in which MTP5 and IAR1 transport metals in an antagonistic fashion to regulate metal homeostasis within the subcellular compartment in which the IAA-conjugate amidohydrolases reside, and support previous suggestions that the ion composition in this compartment influences hydrolase activity.
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DOI: 10.1006/geno.1994.1023
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