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| Title: The IBR5 phosphatase promotes Arabidopsis auxin responses through a novel mechanism distinct from TIR1-mediated repressor degradation .
| | Author: Strader LC Monroe-Augustus M Bartel B | | Journal: BMC Plant Biol Citation: V : 8 P : 41 Year: 2008 Type: MEDLINE | | Literature: oryza Field: abstract Doc ID: pub18423007 Accession (PMID): 18423007 | | Abstract: BACKGROUND : In Arabidopsis , INDOLE-3-BUTYRIC ACID RESPONSE5 ( IBR5 ) , a putative dual-specificity 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 , tir1 , 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 mutant form of IBR5 lacking the catalytic cysteine residue .
CONCLUSION : Our genetic and molecular evidence suggests that IBR5 is a phosphatase that promotes auxin responses , including auxin-inducible transcription , differently than the TIR1 auxin receptor and without destabilizing Aux/IAA repressor proteins .
Our data are consistent with the possibility that auxin-responsive transcription can be modulated downstream of TIR1-mediated repressor degradation .
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[ Sen. 7, subscore: 1.00 ]: 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 mutant form of IBR5 lacking the catalytic cysteine residue .
| | Supplemental links/files: reference in endnote online text related articles pubmed citation | |
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| Title: A gain-of-function mutation in IAA16 confers reduced responses to auxin and abscisic acid and impedes plant growth and fertility .
| | Author: Rinaldi MA Liu J Enders TA Bartel B Strader LC | | Journal: Plant Mol Biol Citation: V : 79 P : 359-73 Year: 2012 Type: MEDLINE | | Literature: oryza Field: abstract Doc ID: pub22580954 Accession (PMID): 22580954 | | Abstract: Auxin regulates many aspects of plant development , in part , through degradation of the Aux/IAA family of transcriptional repressors .
Consequently , stabilizing mutations in several Aux/IAA proteins confer reduced auxin responsiveness .
However , of the 29 apparent Aux/IAA proteins in Arabidopsis thaliana , fewer than half have roles established through mutant analysis .
We identified iaa16-1 , a dominant gain-of-function mutation in IAA16 ( At3g04730 ) , in a novel screen for reduced root responsiveness to abscisic acid .
The iaa16-1 mutation also confers dramatically reduced auxin responses in a variety of assays , markedly restricts growth of adult plants , and abolishes fertility when homozygous .
We compared iaa16-1 phenotypes with those of dominant mutants defective in the closely related IAA7/AXR2 , IAA14/SLR , and IAA17/AXR3 , along with the more distantly related IAA28 , and found overlapping but distinct patterns of developmental defects .
The identification and characterization of iaa16-1 provides a fuller understanding of the IAA7/IAA14/IAA16/IAA17 clade of Aux/IAA proteins and the diverse roles of these repressors in hormone response and plant development .
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[ Sen. 6, subscore: 1.00 ]: We compared iaa16-1 phenotypes with those of dominant mutants defective in the closely related IAA7/AXR2 , IAA14/SLR , and IAA17/AXR3 , along with the more distantly related IAA28 , and found overlapping but distinct patterns of developmental defects .
| | Supplemental links/files: reference in endnote online text related articles pubmed citation | |
