Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1993 Jan;133(1):119-25.
doi: 10.1093/genetics/133.1.119.

Unequal exchange and meiotic instability of disease-resistance genes in the Rp1 region of maize

Affiliations

Unequal exchange and meiotic instability of disease-resistance genes in the Rp1 region of maize

M A Sudupak et al. Genetics. 1993 Jan.

Abstract

The Rp1 region of maize was originally characterized as a complex locus which conditions resistance to the fungus Puccinia sorghi, the causal organism in the common rust disease. Some alleles of Rp1 are meiotically unstable, but the mechanism of instability is not known. We have studied the role of recombination in meiotic instability in maize lines homozygous for either Rp1-J or Rp1-G. Test cross progenies derived from a line that was homozygous for Rp1-J, but heterozygous at flanking markers, were screened for susceptible individuals. Five susceptible individuals were derived from 9772 progeny. All five had nonparental combinations of flanking markers; three had one combination of recombinant flanking markers while the other two had the opposite pair. In an identical study with Rp1-G, 20 susceptible seedlings were detected out of 5874 test cross progeny. Nineteen of these were associated with flanking marker exchange, 11 and 8 of each recombinant marker combination. Our results indicate that unequal exchange is the primary mechanism of meiotic instability of Rp1-J and Rp1-G.

PubMed Disclaimer

References

    1. Genetics. 1985 Sep;111(1):113-30 - PubMed
    1. Mol Gen Genet. 1989 Dec;220(1):140-6 - PubMed
    1. Cell. 1987 May 8;49(3):369-78 - PubMed
    1. Curr Genet. 1987;12(1):1-7 - PubMed
    1. Proc Natl Acad Sci U S A. 1968 Dec;61(4):1300-5 - PubMed

Publication types