Genetic diversity of the mating type and toxin production genes in Pyrenophora tritici-repentis.

Pyrenophora tritici-repentis, the causal agent of tan spot on wheat, is a homothallic loculoascomycete with a complex race structure. The objectives of this study were to confirm the homothallic nature of the pathogen, characterize mating type diversity and toxin production genes in a global collection of strains, and analyze how these traits are associated between each other and with existing races. The pseudothecia production capacity, race identification, mating type locus (MAT), internal transcribed spacer, and glyceraldehyde-3-phosphate dehydrogenase regions were analyzed in a selection of 88 strains originating from Europe, North and South America, North Africa, and Central and South Asia. Some (60%) strains produced pseudothecia containing ascospores, independent of their origin. Race identification obtained using the multiplex polymerase chain reaction targeting host-selective toxin (HST) genes was consistent, overall, with the results based on the inoculation of a set of differential wheat cultivars and confirmed the predominance of race 1/2 strains ( approximately 83%). However, discrepancies in race identification, differences from the reference tester strains, and atypical ToxA profiles suggest the presence of new races and HSTs. The MAT1-1 and MAT1-2 coding regions are consecutively arranged in a single individual, suggesting putative heterothallic origin of P. tritici-repentis. Upstream from the MAT is an open reading frame of unknown function (ORF1) containing a MAT-specific degenerate carboxy-terminus. The phylogenetic analysis of the MAT locus reveals two distinct groups, unlinked to geographical origin or ToxA profile. Group I, the best-represented group, is associated with typical tan spot lesions caused by races 1, 2, 3, and 5 on wheat. It is more homogenous than group II encompassing race 4 strains, as well as isolates associated primarily with small spot lesions on wheat leaves or other hosts. Group II could contain several distinct taxa.

Spermine and spermidine induce intestinal maturation in the rat.

In the present study, we aimed to induce precocious intestinal maturation in neonatal rats by the oral administration of polyamines. Groups of 5 rats received either saline, spermidine (10 mumol daily), or spermine (6 mumol daily) orally on the 12th, 13th, and 14th postnatal days. The rats were killed on the 15th postnatal day. After the small bowel was removed, a 1-cm distal ileal segment was removed for histologic examination and the remaining small bowel tissue was homogenized for further biochemical analysis. Polyamine administration was shown to induce structural and biochemical mucosal changes characteristic of postnatal maturation. Lactase, sucrase, and maltase specific activities (micromoles of substrate hydrolyzed per minute per gram of protein) were 80 +/- 10, 10 +/- 3, and 116 +/- 19 for the saline-treated rats; 51 +/- 7, 34 +/- 2, and 315 +/- 37 for the spermidine-treated rats; and 25 +/- 2, 46 +/- 5, and 419 +/- 63 for the spermine-treated rats, respectively. Similar results were obtained with rats, first treated with spermine (6 mumol) on the 7th postnatal day, receiving spermine (6 mumol) daily as described above and killed on the 10th postnatal day. Dose-response experiments performed as reported above in rats whose treatment began on the 12th postnatal day showed that the maturational effects of orally administered spermine are dose-dependent.

Chromosomes involved in production of infectious SV40 particles in mouse/SV40-transformed Chinese hamster cell hybrids.

The clone 6d hybrid, capable of expressing the virus-specific T-antigen but unable to produce infectious virus particles after superinfection, presented a complete mouse (3T3-4E) chromosome complement and a significant loss of Chinese hamster (CHK/SVLP AG) chromosomes. Similar properties were displayed by a BUdR-resistant derivative of the Cl 6d hybrid (Cl 6d.6BU). Three independent superhybrid clones (CL 10B, Cl 10C, Cl 11A) isolated after backcross of the Cl 6d.6BU hybrid with a nontransformed Chinese hamster kidney cell line (CHK/AG) were able to produce infectious SV40 virus. In spite of the loss of mouse chromosomes, there was no significant difference in the average number of chromosomes between the Cl 6d.6BU and the superhybrid clones. Thus, the Chinese hamster chromosomes seemed to compensate for the loss of the mouse chromosomes. Although the effect of Chinese hamster chromosomes cannot be totally disregarded, our data suggested a positive correlation between the inability to produce infectious SV40 and the presence of certain mouse chromosomes.