First published online January 30, 2003; 10.1104/pp.015677
Plant Physiol, March 2003, Vol. 131, pp. 998-1008
Dual Genetic Pathways Controlling Nodule Number in
Medicago truncatula1
R. Varma
Penmetsa,2
Julia A.
Frugoli,3
Lucinda S.
Smith,
Sharon R.
Long, and
Douglas R.
Cook2*
Department of Plant Pathology and Microbiology, Texas A&M
University, College Station, Texas 77843 (R.V.P., J.A.F., D.R.C.); and
Department of Biological Sciences, Stanford University, Stanford,
California 94305 (L.S.S., S.R.L.)
We report the isolation and characterization of a new
Medicago truncatula hyper-nodulation mutant, designated
sunn (super numeric nodules). Similar to the previously
described ethylene-insensitive mutant sickle,
sunn exhibits a 10-fold increase in the number of
nodules within the primary nodulation zone. Despite this general similarity, these two mutants are readily distinguished based on
anatomical, genetic, physiological, and molecular criteria. In contrast
to sickle, where insensitivity to ethylene is thought to
be causal to the hyper-nodulation phenotype (R.V. Penmetsa, D.R. Cook
[1997] Science 275: 527-530), nodulation in sunn is normally sensitive to ethylene. Nevertheless, sunn
exhibits seedling root growth that is insensitive to ethylene, although
other aspects of the ethylene triple response are normal; these
observations suggest that hormonal responses might condition the
sunn phenotype in a manner distinct from
sickle. The two mutants also differ in the anatomy of
the nodulation zone: Successful infection and nodule development in
sunn occur predominantly opposite xylem poles, similar
to wild type. In sickle, however, both infection and
nodulation occur randomly throughout the circumference of the
developing root. Genetic analysis indicates that sunn
and sickle correspond to separate and unlinked loci,
whereas the sunn/skl double mutant exhibits a novel and
additive super-nodulation phenotype. Taken together, these results
suggest a working hypothesis wherein sunn and
sickle define distinct genetic pathways, with
skl regulating the number and distribution of successful
infection events, and sunn regulating nodule organogenesis.
1
This work was supported by the Samuel Roberts
Noble Foundation (Ardmore, OK; grant), by the Human Frontiers Science
Program (grant no. RG-0327), by the U.S. National Science Foundation
(grant no. IBN 9507535 to D.R.C.), and by the College of Agriculture and Life Sciences, Texas A&M University (Tom Slick Graduate Fellowship to R.V.P.).
2
Present address: Department of Plant Pathology,
University of California, Davis, CA 95616-8680.
3
Present address: Department of Genetics and
Biochemistry, Clemson University, Clemson, SC 29634.
*
Corresponding author; e-mail drcook{at}ucdavis.edu; fax
530-752-5674.
© 2003 American Society of Plant Biologists
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