Degree Type


Date of Award


Degree Name

Doctor of Philosophy


Zoology and Genetics

First Advisor

Patrick S. Schnable


An autonomous Cy transposable element of Zea mays inserted at the a1 locus (a1-m5216: MuDR) was isolated genetically and molecularly cloned. Restriction mapping and sequencing results indicate that Cy (designated MuDR:Cy1) is another isolate of the autonomous element of the Mutator family, MuDR. Six defective derivative alleles of a1-m5216:MuDR were isolated genetically and molecularly cloned. Five of these a1-r alleles (a1-r5835, a1-r5431, a1-r182, a1-r5938 and a1-r5306) behave like non-autonomous elements in that their transposition can only be activated by active MuDR elements in trans. Three of these a1-r alleles have deletions that disrupt transcript mudrA. One allele has a deletion that disrupts transcript mudrB. The lesion associated with the remaining a1-r allele could disrupt either mudrA or mudrB, or both. Analysis of the a1-r alleles results suggests that both transcripts encoded by active MuDR elements, mudrA and mudrB, are necessary for autonomous transposition. The sixth allele, a1-nr5940, which does not respond to the activation of active MuDR elements, has a deletion involving transcript mudrA, the 5' terminal inverted repeat of MuDR and a1 coding sequence. The origin of the a1-r and a1-nr alleles can be explained by the gap-repair model. Another MuDR:Cy element (designated MuDR:Cy2 and which maps 10 cM distal of the pr1 locus on chromosome 5) was shown to transpose at a rate of 3.3% of gametes per generation and increase its copy numbers at rates from 0 to 28.6% of MuDR-containing gametes. Genetic and molecular tests in inactive Mutator lines demonstrated that an active MuDR:Cy2 element can restore the Mu1 hypomethylation and reactivate the high forward mutation rate associated with active Mutator lines. The subsequent loss of MuDR:Cy2 via meitotic segregation resulted in increased levels of Mu1 methylation. Analysis of a novel change of state of a Mu element insertion mutation at the bz1 locus (bz1-rcy4333y) revealed that developmental regulation of MuDR activity is not responsible for the unique insertion and excision patterns associated with Mu elements. Instead, a model involving developmentally regulated gap-repair is proposed.



Digital Repository @ Iowa State University,

Copyright Owner

An-Ping Hsia



Proquest ID


File Format


File Size

121 pages

Included in

Genetics Commons