ArticleGenetics1997
Mu element-generated gene conversions in maize attenuate the dominant knotted phenotype.
Article in Genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Independent evolution of transposase and TIRs facilitated by recombination betweenProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Distal expression of knotted1 in maize leaves leads to reestablishment of proximal/distal patterning and leaf dissection.Plant physiology · 2009Article
- MuDR transposase increases the frequency of meiotic crossovers in the vicinity of a Mu insertion in the maize a1 gene.Genetics · 2005Article
- Ac insertion site affects the frequency of transposon-induced homologous recombination at the maize p1 locus.Genetics · 2000Article
- Knots in the family tree: evolutionary relationships and functions of knox homeobox genes.Plant molecular biology · 2000Review
- The evolution of disease resistance genes.Plant molecular biology · 2000Review
- Gnarley1 is a dominant mutation in the knox4 homeobox gene affecting cell shape and identity.The Plant cell · 1999Article
- Epigenetic interactions among three dTph1 transposons in two homologous chromosomes activate a new excision-repair mechanism in petunia.The Plant cell · 1999Article
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The knotted1 gene was first defined by dominant mutations that affect leaf morphology. The original allele, Kn1-O, results from a 17-kb tandem duplication. Mutator (Mu) insertions near the junction of the two repeats suppress the leaf phenotype to different degrees depending on the position of the insertion. The Mu insertions also increase the frequency of recombination at Kn1-O to create derivative alleles in which the Mu element and one copy of the repeat are lost. These derivatives are normal in appearance. Here we describe two derivatives that retained the tandem duplication but gained insertions of 1.7 and 3 kb in length in place of the Mu element. In each case, the inserted DNA is a sequence that normally flanks the distal repeat unit. Thus, each derivative consists of a tandem duplication in which the repeat unit has been extended at its distal end by the length of the new insertion. The 1.7-kb insertion dampens the phenotype, as did the original Mu insertion, whereas the 3-kb insertion completely suppresses the knotted phenotype. We propose that gene conversion, stimulated by the double-strand break of the Mu excision, gave rise to these derivatives.
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