Plant Genome I Conference
Town & Country Conference Center, San Diego, CA, November, 1992.
PG-I: 5pg1
SATURATING THE LINKAGE MAP OF ARABIDOPSIS THALIANA WITH
EMBRYONIC MUTATIONS.
Linda Franzmann, Elizabeth Yoon, and David Meinke, Department of
Botany,Oklahoma State University, Stillwater,OK 74078.
The value of saturating genetic maps with visible markers
has been demonstrated in a variety of experimental organisms.
The mapping project outlined in this poster was designed to
enhance the linkage map of Arabidopsis, complement the large
multinational effort to characterize the Arabidopsis genome, and
establish a valuable resource of recessive embryonic mutants
defective in genes with known chromosomal locations. Our
approach has been to determine recombination frequencies between
embryonic mutations and visible markers [D.A. Patton, L.H.
Franzmann, and D.W. Meinke, Mol. Gen. Genet. 227, 337-347
(1991)]. We have isolated and characterized 250 emb mutants of
Arabidopsis defective in embryo development. This collection
includes 178 mutants generated by Ken Feldmann following seed
transformation. Forty three of these mutants appear to be tagged
with T-DNA. We have now assigned 85 emb mutants to linkage
groups and placed 40% of these mutants on the linkage map.
Embryo-defective mutants are therefore without question the most
common class of morphological marker on the linkage map of
Arabidopsis. We hope to map the chromosomal locations of 100
total genes. Insertional mutants will be particularly useful for
integrating the classical and molecular maps. Six tagged mutants
unexpectedly exhibited linkage to visible markers on more than
one chromosome. These mutants appear to contain chromosomal
translocations associated with the site of T-DNA insertion. A
significant percentage of mutants obtained from Ken Feldmann's
lines may therefore contain plant chromosomal rearrangements.
These translocations will be particularly valuable if the break
point is associated with both a mutant phenotype (embryonic
defect) and a molecular (T-DNA)marker.
This research has been supported by NSF grant # DIR-9104215.
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