All-Russia Research Institute for Agricultural Microbiology
189620, St. Petersburg
Pushkin 8, Podbelsky sh. 3, Russia
A wide-range panel of pea mutants impaired in nitrogen-fixing symbiosis have been analyzed for their ability to form arbuscular endomycorrhiza (AM) with the result that some were also found to be unable to form AM (Myc– phenotype) [1,3,4,7]. Several additional nitrogen-fixing symbiosis mutants have been obtained from cv. Rondo: K5 and K24 are non-nodulating mutants, nod3 is supernodulating mutant and FN1 is non-fixing and supernodulating mutant [5,6,9].
We decided to perform investigations similar to those described above on these latter mutants (the seeds were kindly provided by Prof. E. Jacobsen, Agricultural University, Wageningen, The Netherlands). We found that none of the mutants differed from parental cv. Rondo in their ability to form AM. The fact that mutant K24 was able to form AM appears to contradict data in the literature. It was reported that mutant K24 is allelic to mutant NEU5 at the sym19 locus [12]. It was also shown that allelic mutants P6 and P55 induced on cv. Frisson [2,11] represent mutations at sym19 and display a Myc– phenotype [3,10]. Finally, these three mutants were described as having different phenotypes with respect to nitrogen-fixing symbiosis: K24 was described as mutant impaired in infection thread formation (Hac+Inf– phenotype) [8], whereas mutants P6 and P55 are impaired at earlier stage of symbiosis development (Hac–Inf– phenotype) [10].
Because our results were counter to what was predicted from the literature, we decided to conduct direct allelism test between mutant K24 and other mutants supposed to be mutants at the sym19 locus. The tests have been performed and mutant K24 turned to be non-allelic to mutants P6 and NEU5. Thus, mutant K24 is not an allele of sym19.
Acknowledgments: This work was financially supported by Russian Fund for Basic Research (97-04-50033).
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