Symbiotic seed germination and protocorm development of Aa achalensis Schltr., a terrestrial orchid endemic from Argentina

Aa achalensis is an endangered terrestrial orchid endemic from Argentina. In vitro symbiotic seed germination was evaluated for its propagation. Five different fungal strains were isolated from this species: two Rhizoctonia-like related to Thanatephorus cucumeris and three ascomicetaceous fungi belonging to Phialophora graminicola and one to an uncultured Pezizaceae. All five isolates promoted seed germination being one T. cucumeris strain the most effective. After 16 weeks of growth, 30 % of A. achalensis protocorms developed until seedlings with two/four leaves in this treatment. These findings open an opportunity to the knowledge and preservation of this species.     

Studies on several genetic hematological traits of the Mexican population. XVI. Hemoglobin, S and glucose-6-phosphate dehydrogenase deficiency in the east coast

The distribution of abnormal hemoglobins, glucose-6-phosphate dehydrogenase deficiency, blood group antigens A, B, M, N, C, c, D, E, e, V, Duffy and Diego, serum haptoglobins, transferrins and pseudocholinesterase types, were investigated in five villages of the East Coast of Mexico, where vivax malaria was endemic until recently. Hemoglobin S and G-6-PD deficiency were present in variable degrees in all five locations. All patients with the enzyme deficiency had the A band by electrophoresis, which coupled with the presence of hemoglobin C and haptoglobin 2-1 M in a few individuals strongly suggested Negro admixture. The high frequency of antigen V and the relatively low frequency of Fy (a +) were congruent with the above hypothesis and the conclusion was drawn that the presence of hemoglobin S and G-6-PD deficiency in this area is due to Negro admixture. Unusually high frequencies of the Diego antigen were observed in three of the five villages studied.     

Role of the RecBCD Recombination Pathway in Salmonella Virulence

Mutants of Salmonella enterica lacking the RecBC function are avirulent in mice and unable to grow inside macrophages (N. A. Buchmeier, C. J. Lipps, M. Y. H. So, and F. Heffron, Mol. Microbiol. 7:933-936, 1993). The virulence-related defects of RecBC(-) mutants are not suppressed by sbcB and sbcCD mutations, indicating that activation of the RecF recombination pathway cannot replace the virulence-related function(s) of RecBCD. Functions of the RecF pathway such as RecJ and RecF are not required for virulence. Since the RecBCD pathway, but not the RecF pathway, is known to participate in the repair of double-strand breaks produced during DNA replication, we propose that systemic infection by S. enterica may require RecBCD-mediated recombinational repair to prime DNA replication inside phagocytes. Mutants lacking both RecD and RecJ are also attenuated in mice and are unable to proliferate in macrophages, suggesting that exonucleases V and IX provide alternative functions for RecBCD-mediated recombinational repair during Salmonella infection.