First published online November 26, 2002; 10.1105/tpc.006338
The Plant Cell, Vol. 14, 3213-3223,
December 2002, Copyright © 2002,
American Society of Plant Biologists
Structural Analysis of the Maize Rp1 Complex Reveals Numerous Sites and Unexpected Mechanisms of Local Rearrangement
Wusirika Ramakrishnaa,
John Embertona,
Matthew Ogdena,
Phillip SanMiguelb and
Jeffrey L. Bennetzen1,a
a Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907
b Purdue University Genomics Core, Purdue University, West Lafayette, Indiana 47907
1 To whom correspondence should be addressed. E-mail maize{at}bilbo.bio.purdue.edu; fax 765-496-1496
Rp1 is a complex disease resistance locus in maize that is exceptional in both allelic variability and meiotic instability. Genomic sequence analysis of three maize BACs from the Rp1 region of the B73 inbred line revealed 4 Rp1 homologs and 18 other gene-homologous sequences, of which at least 16 are truncated. Thirteen of the truncated genes are found in three clusters, suggesting that they arose from multiple illegitimate break repairs at the same sites or from complex repairs of each of these sites with multiple unlinked DNA templates. A 43-kb region that contains an Rp1 homolog, six truncated genes, and three Opie retrotransposons was found to be duplicated in this region. This duplication is relatively recent, occurring after the insertion of the three Opie elements. The breakpoints of the duplication are outside of any genes or identified repeat sequence, suggesting a duplication mechanism that did not involve unequal recombination. A physical map and partial sequencing of the Rp1 complex indicate the presence of 15 Rp1 homologs in regions of 250 and 300 kb in the B73 inbred line. Comparison of fully sequenced Rp1-homologous sequences in the region demonstrates a history of unequal recombination and diversifying selection within the Leu-rich repeat 2 region, resulting in chimeric gene structures.
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