Plant Gene Expression Center
University of California

Mapping of the dominant Fascicled locus and generation of revertants
--Jackson, D*, Hake, S
*Current address: Cold Spring Harbor Lab., PO Box 100, Cold Spring Harbor, NY 11724

The dominant Fascicled (Fas1) mutation causes enlargement and splitting of the primary inflorescence apical meristems. Fas1 plants have huge branched ears and split central tassel branches (Figure, normal ear on left, Fas1 ear on right). The ontogeny of Fas1 inflorescences has been characterized in detail by Orr and co-workers (Orr, Haas and Sundberg, AJB 84:723-34, 1997).

We mapped Fas1 using the standard set of waxy reciprocal translocations. Fas1 plants (Wx1) were crossed to each translocation tester and F1 Fas1 plants were crossed by wx1 testers. Analysis of the F2 progeny from several different translocation crosses indicated that Fas1 was in repulsion to wx1, suggesting that Fas1 is on chromosome 9. To confirm this we crossed Fas1 by Rolled, and outcrossed the double mutants to standard inbreds. In the F2, we found that Fas1 was in repulsion to Rld1, (38 +/+; 89 Fas/+; 85 +/Rld; 27 Rld/Fas individuals) indicating a map distance of approximately 27 cM between Rld1 and Fas1. Since Rld1 is close to the distal tip of 9L, and we know that Fas1 is linked to wx1, it is most likely that Fas1 is proximal to Rld1 and we tentatively place it at 9L-110+/-.

In an attempt to characterize the molecular lesion in the Fas1 locus, we screened for Mutator induced revertants. Mu active, homozygous Fas1 plants were crossed by normal pollen from the W23 inbred line, and we screened for plants with normal ears and tassels in the F1 generation. In a small pilot screen we recovered five normal plants in a population of only seven thousand plants, a frequency much higher than expected for a targeted Mu insertion. Since Fas1 plants were used as the female parent in the initial crosses it is unlikely that the normal plants were the result of contamination. Test crossing of the putative revertants gave plants with normal inflorescences, and we did not see any new recessive phenotypes segregating in the self progeny.

The high frequency of reversion of the Fas1 locus is similar to the frequency observed for revertants of the dominant Knotted1-O allele. Kn1-O is caused by a tandem duplication and many of the revertants resulted from loss of the duplicated copy rather than transposon insertion (Veit et al., Genetics 125:623-31, 1990). If a similar phenomenon is causing reversion of the dominant Fas1 phenotype, it may not be possible to isolate the Fas1 gene by this strategy.

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