Because soybean [Glycine max (L.) Merr.] are generally assumed to be active in N, fixation, their genetic variation in this trait has not been studied to the extent found in other crop legumes. In the few studies undertaken, local cultivars of limited genetic diversity have dominated. This study considered the genetic variation in N2 fixation of 21 Group 00 and 27 Group 0 soybean plant introductions over 2 yr at two Minnesota locations [Hubbard loamy sand (sandy, mixed Udorthetic Haploborall) and Waukegan silt loam (fine‐silty over sandy, mixed, mesic Typic Hapludoll)] differing in available soil N. Traits measured were total N2 fixed (estimated by the difference method using a Clay Maturity Group 0 non‐nodulating line), shoot dry weight at R2 and R6, plant N concentration at R6, the proportion of plant N derived from fixation, and seed yield. All traits except N concentration were positively and highly correlated with total N2 fixed, and therefore have the potential to be used as indirect estimates of N2 fixation for field screening under low to moderate soil N conditions. There were significant differences within both maturity groups for all traits. Some Group 00 lines fixed more N, than ‘McCall’ and as much N, as high N2‐fixing Maturity Group 0 lines. There was sufficient genetic variation to suggest that breeding for improved N2 fixation is feasible in both maturity groups.
The original version of this Article contained an error in the spelling of a member of the PRACTICAL Consortium, Manuela Gago-Dominguez, which was incorrectly given as Manuela Gago Dominguez. This has now been corrected in both the PDF and HTML versions of the Article. Furthermore, in the original HTML version of this Article, the order of authors within the author list was incorrect. The PRACTICAL consortium was incorrectly listed after Richard S. Houlston and should have been listed after Nora Pashayan. This error has been corrected in the HTML version of the Article; the PDF version was correct at the time of publication.
Prostate cancer appears to result from complex interactions among genetic, endocrine and environmental factors. Identi®cation of risk factors for development and progression of prostate cancer is needed. This will allow researchers to design strategies to reduce the morbidity and mortality from this cancer and to identify individuals at increased risk of developing the disease. It is probable that common genetic polymorphisms (variants) in genes directly and indirectly involved in androgen biosynthesis, metabolism and regulation are important. Other important genes are likely to be those directly involved in regulation of prostate cell proliferation and apoptosis. Prostate Cancer and Prostatic Diseases (2000) 3, 236±240.
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