Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: The IBR5 phosphatase promotes Arabidopsis auxin responses through a novel mechanism distinct from TIR1-mediated repressor degradation | BMC Plant Biology BioMed Central Research article Open Access The IBR5 phosphatase promotes Arabidopsis auxin responses through a novel mechanism distinct from TIR1-mediated repressor degradation Lucia C Strader Melanie Monroe-Augustus and Bonnie Bartel Address Department of Biochemistry and Cell Biology Rice University Houston Texas 77005 USA Email Lucia C Strader - strader@ Melanie Monroe-Augustus - melaniem@ Bonnie Bartel - bartel@ Corresponding author Published 18 April 2008 Received 2 October 2007 BMC Plant Biology 2008 8 41 doi 1471-2229-8-41 Accepted 18 April 2008 This article is available from http 1471-2229 8 41 2008 Strader et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background In Arabidopsis INDOLE-3-BUTYRIC ACID RESPONSE5 IBR5 a putative dualspecificity protein phosphatase is a positive regulator of auxin response. Mutations in IBR5 result in decreased plant height defective vascular development increased leaf serration fewer lateral roots and resistance to the phytohormones auxin and abscisic acid. However the pathways through which IBR5 influences auxin responses are not fully understood. Results We analyzed double mutants of ibr5 with other mutants that dampen auxin responses and found that combining ibr5 with an auxin receptor mutant tirl enhanced auxin resistance relative to either parent. Like other auxin-response mutants auxin-responsive reporter accumulation was reduced in ibr5. Unlike other auxin-resistant mutants the Aux IAA repressor reporter protein AXR3NT-GUS was not stabilized in ibr5. Similarly the Aux IAA repressor IAA28 was less abundant in ibr5 than in wild type. ibr5 defects were not fully rescued by overexpression of a .
