Originally published as Genetics Published Articles Ahead of Print on February 9, 2009.

Genetics, Vol. 181, 1229-1237, April 2009, Copyright © 2009
doi:10.1534/genetics.108.093666

Disruption of Imprinting by Mutator Transposon Insertions in the 5' Proximal Regions of the Zea mays Mez1 Locus

William J. Haun*, Olga N. Danilevskaya{dagger}, Robert B. Meeley{dagger} and Nathan M. Springer*,1

* Microbial and Plant Genomics Institute, Department of Plant Biology, University of Minnesota, St. Paul, Minnesota 55108 and {dagger} Pioneer Hi-Bred International, Johnston, Iowa 50131

1 Corresponding author: Department of Plant Biology, University of Minnesota, 250 Biological Sciences Center, 1445 Gortner Ave., St. Paul, MN 55108.
E-mail: springer{at}umn.edu

Imprinting is a form of epigenetic gene regulation in which alleles are differentially regulated according to the parent of origin. The Mez1 gene in maize is imprinted such that the maternal allele is expressed in the endosperm while the paternal allele is not expressed. Three novel Mez1 alleles containing Mutator transposon insertions within the promoter were identified. These mez1-mu alleles do not affect vegetative expression levels or result in morphological phenotypes. However, these alleles can disrupt imprinted expression of Mez1. Maternal inheritance of the mez-m1 or mez1-m4 alleles results in activation of the normally silenced paternal allele of Mez1. Paternal inheritance of the mez1-m2 or mez1-m4 alleles can also result in a loss of silencing of the paternal Mez1 allele. The paternal disruption of imprinting by transposon insertions may reflect a requirement for sequence elements involved in targeting silencing of the paternal allele. The maternal disruption of imprinting by transposon insertions within the Mez1 promoter suggests that maternally produced MEZ1 protein may be involved in silencing of the paternal Mez1 allele. The endosperms with impaired imprinting did not exhibit phenotypic consequences associated with bi-allelic Mez1 expression.


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Genetics 2009 181: NP. [Full Text]