Persistent Link:
http://hdl.handle.net/10150/194275
Title:
Tandem Repeats are Sufficient for b1 Paramutation
Author:
Belele, Christiane
Issue Date:
2006
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Paramutation is an allele interaction that causes a heritable change in the expression of one allele. At the b1 locus an interaction between B' and B-I alleles results in a change of B-I to B', symbolized by B'*. A combination of fine-structure mapping and transgenic approaches have demonstrated that the tandem repeats located ~100 kb upstream of the b1 transcription start site are sufficient for both paramutation and high expression.Plants carrying transgenes with tandem repeats in ectopic locations (repeat-transgene) were able to change B-I into B'*. The B'* state induced by the repeat-transgene was heritable and paramutagenic when segregated from the repeat-transgene. In addition, the repeat-transgene induced B-I silencing was prevented by the trans-acting mutation required for paramutation mop1-1, which was recently found to encode a RNA-dependent RNA polymerase (RdRP). Transgenes containing seven tandem repeats of only the 5' half of the sequence were able to paramutate B-I. Taken together, these results demonstrate that the paramutation sequences are contained in the 5' half of the repeats and they can paramutate B-I from non-allelic positions. Because paramutation induced by the repeat-transgenes and the endogenous B' allele are both heritable and depend on a functional RdRP, they likely involve a similar mechanism of RNA-mediated chromatin modification.Furthermore, we found that the tandem repeats are also sufficient for high expression of the b1 gene. When fused to a GUS reporter gene and introduced into maize, the tandem repeats enhanced GUS expression above the level observed for GUS transgenes that did not have the repeats. As observed with the endogenous B-I allele, the enhancer function of the repeats in the GUS transgenes is silenced by B' and the paramutagenic repeat-transgenes. After being with B' or the paramutagenic repeat-transgenes the repeats in the GUS constructs lost their ability to enhance gene expression.The identification of the tandem repeats as the sequences mediating paramutation suggest a new function for tandem repeats, mediating trans-interactions to establish heritable epigenetic states. Models are discussed for how alleles might communicate in trans to establish different epigenetic states and how the epigenetic state is maintained through mitosis and meiosis.
Type:
text; Electronic Dissertation
Keywords:
epigenetics; paramutation; b1 gene
Degree Name:
PhD
Degree Level:
doctoral
Degree Program:
Plant Science; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Chandler, Vicki L.
Committee Chair:
Chandler, Vicki L.

Full metadata record

DC FieldValue Language
dc.language.isoENen_US
dc.titleTandem Repeats are Sufficient for b1 Paramutationen_US
dc.creatorBelele, Christianeen_US
dc.contributor.authorBelele, Christianeen_US
dc.date.issued2006en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractParamutation is an allele interaction that causes a heritable change in the expression of one allele. At the b1 locus an interaction between B' and B-I alleles results in a change of B-I to B', symbolized by B'*. A combination of fine-structure mapping and transgenic approaches have demonstrated that the tandem repeats located ~100 kb upstream of the b1 transcription start site are sufficient for both paramutation and high expression.Plants carrying transgenes with tandem repeats in ectopic locations (repeat-transgene) were able to change B-I into B'*. The B'* state induced by the repeat-transgene was heritable and paramutagenic when segregated from the repeat-transgene. In addition, the repeat-transgene induced B-I silencing was prevented by the trans-acting mutation required for paramutation mop1-1, which was recently found to encode a RNA-dependent RNA polymerase (RdRP). Transgenes containing seven tandem repeats of only the 5' half of the sequence were able to paramutate B-I. Taken together, these results demonstrate that the paramutation sequences are contained in the 5' half of the repeats and they can paramutate B-I from non-allelic positions. Because paramutation induced by the repeat-transgenes and the endogenous B' allele are both heritable and depend on a functional RdRP, they likely involve a similar mechanism of RNA-mediated chromatin modification.Furthermore, we found that the tandem repeats are also sufficient for high expression of the b1 gene. When fused to a GUS reporter gene and introduced into maize, the tandem repeats enhanced GUS expression above the level observed for GUS transgenes that did not have the repeats. As observed with the endogenous B-I allele, the enhancer function of the repeats in the GUS transgenes is silenced by B' and the paramutagenic repeat-transgenes. After being with B' or the paramutagenic repeat-transgenes the repeats in the GUS constructs lost their ability to enhance gene expression.The identification of the tandem repeats as the sequences mediating paramutation suggest a new function for tandem repeats, mediating trans-interactions to establish heritable epigenetic states. Models are discussed for how alleles might communicate in trans to establish different epigenetic states and how the epigenetic state is maintained through mitosis and meiosis.en_US
dc.typetexten_US
dc.typeElectronic Dissertationen_US
dc.subjectepigeneticsen_US
dc.subjectparamutationen_US
dc.subjectb1 geneen_US
thesis.degree.namePhDen_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePlant Scienceen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorChandler, Vicki L.en_US
dc.contributor.chairChandler, Vicki L.en_US
dc.contributor.committeememberJorgensen, Richarden_US
dc.contributor.committeememberLarkins, Brianen_US
dc.contributor.committeememberYadegari, Raminen_US
dc.contributor.committeememberVierling, Elizabethen_US
dc.identifier.proquest1864en_US
dc.identifier.oclc659746418en_US
All Items in UA Campus Repository are protected by copyright, with all rights reserved, unless otherwise indicated.