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First published online January 30, 2003; 10.1104/pp.015677

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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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