DNA G-quartets in a 1.86 A resolution structure of an Oxytricha nova telomeric protein-DNA complex.

The Oxytricha nova telomere end binding protein (OnTEBP) recognizes, binds and protects the single-stranded 3'-terminal DNA extension found at the ends of macronuclear chromosomes. The structure of this complex shows that the single strand GGGGTTTTGGGG DNA binds in a deep cleft between the two protein subunits of OnTEBP, adopting a non-helical and irregular conformation. In extending the resolution limit of this structure to 1.86 A, we were surprised to find a G-quartet linked dimer of the GGGGTTTTGGGG DNA also packing within the crystal lattice and interacting with the telomere end binding protein. The G-quartet DNA exhibits the same structure and topology as previously observed in solution by NMR with diagonally crossing d(TTTT) loops at either end of the four-stranded helix. Additionally, the crystal structure reveals clearly visible Na(+), and specific patterns of bound water molecules in the four non-equivalent grooves. Although the G-quartet:protein contact surfaces are modest and might simply represent crystal packing interactions, it is interesting to speculate that the two types of telomeric DNA-protein interactions observed here might both be important in telomere biology.     

Host-specific regulation of nodulation genes in Rhizobium is mediated by a plant-signal, interacting with the nodD gene product

We have identified a nodD gene from the wide host-range Rhizobium strain MPIK3030 (termed nodD1) which is essential for nodulation on Macroptilium atropurpureum (siratro). Experiments with nodA–lacZ gene fusions demonstrate that the MPIK3030 nodD1 regulates expression of the nodABC genes. Additionally, we used nodC–lacZ fusions of Rhizobium meliloti to show that the MPIK3030 nodD1 gene induces expression of these fusions by interacting with plant factors from siratro and from the non-host Medicago sativa (alfalfa). The R. meliloti nodD genes, however, only interact with alfalfa exudate. In line with these results, no complementation of MPIK3030 nodD1 mutants could be obtained on siratro with the R. meliloti nodD genes, while the MPIK3030 nodD1 can complement nodD mutants of R. meliloti on alfalfa. Furthermore, R. meliloti transconjugants harbouring the MPIK3030 nodD1 efficiently nodulate the illegitimate host siratro. When compared with other nodD sequences, the amino acid sequence of the MPIK3030 nodD1 shows a conserved aminoterminus, whereas the carboxy-terminus of the putative gene product diverges considerably. Studies on a chimeric MPIK3030/R. meliloti nodD gene indicates that the carboxy-terminal region is responsible for the interaction with plant factor(s) and may have evolved in different rhizobia specifically to interact with plant–host factors.     

The inhibitory effect of succinate on radiation-enhanced mitochondrial lipid peroxidation

The degree of mitochondrial ADP/Fe/NADPH-induced lipid peroxidation was increased up to the fourth day after 9.0 Gy whole body gamma-irradiation. The lipid peroxidation inhibiting effect of succinate added to isolated mitochondria was diminished as a consequence of irradiation. The succinate, administered in vivo prior to irradiation, decreased the amount of malondialdehyde production and protected the succinate dehydrogenase enzyme against inactivation. The mean survival of succinate-pretreated animals was much longer than that of controls. The role of mitochondrial lipid peroxidation in the pathogenesis of radiation injury is discussed.     

Lipid peroxidation in Ehrlich ascites cell mitochondria is not determined by the polyunsaturated fatty acid content of the membrane

Lipid peroxidation intensity is compared in Ehrlich Ascites Cell and in liver mitochondria, prepared from tumor bearing mice. Malondialdehyde formation is negligible in intact ascites tumour mitochondria, but it is significantly increased in permeabilised mitochondria and in isolated mitochondrial membranes. We suggest that the resistance against oxidative stress is a consequence of efficient protective mechanisms operating in the intact tumour mitochondria and the low level of polyunsaturated fatty acids under these circumstances cannot be the rate limiting factor in lipid peroxidation. Succinate, an effective inhibitor of mitochondrial lipid peroxidation in liver, cannot determine malondialdehyde formation in ascites tumour mitochondria.     

Diversity of coding strategies in influenza viruses.

Influenza viruses have exploited a variety of strategies to increase their genome coding capacities. These include unspliced, spliced, alternatively spliced and bicistronic mRNAs, translation from overlapping reading frames and a coupled stop-start translation of tandem cistrons.     

The choice between two distinct T cell determinants within a 23-amino acid region of lysozyme depends on their structural context

The specificity of C57BL/6 T cells reactive to peptide aa 74-96 of hen egg-white lysozyme (HEL) was analyzed by using a panel of synthetic peptides of varying lengths from this region. It was found that peptide 74-96-reactive T cells induced by native HEL (aa 1-129) or its denatured fragment L2 (aa 13-105) recognized two distinct but overlapping determinants contained within aa 74-90 or aa 81-96, respectively. Peptide 74-96 itself induced both peptide 74-90-and peptide 81-96-specific T cells. Thus, a choice was made between these two potential T cell determinants on peptide 74-96, depending on which immunogen was used. Interestingly, the ability of both peptide determinants aa 74-90 and aa 81-96 to stimulate peptide 74-96-reactive T cells was partly dependent on the presence of residues within the overlap region (aa 81-90), suggesting that this region may play an important role in Iab-restricted T cell activation. This was further supported by the poor immunogenicity of shorter peptides 74-86 or 85-96, lacking residues from the overlap region in B6 mice. These two short peptides were nevertheless capable of eliciting T cell responses in B10.A mice, suggesting that the importance of this overlap region in obtaining a response to peptide 74-96 is related to the MHC haplotype.     

SALT REGULATION AND LEAF SENESCENCE IN AGING LEAVES OF JAUMEA CARNOSA (LESS.) GRAY (ASTERACEAE), A SALT MARSH SPECIES EXPOSED TO NaCl STRESS

The effects of increasing salt stress on leaf senescence and salt regulation were investigated in the halophyte Jaumea carnosa in hydroponic culture experiments. The plants were grown in Hoagland's nutrient solution plus additional NaCl salt (0, 300, 400, 500 mm NaCl). Decreases in nucleic acids, protein, and chlorophyll were used as indicators of leaf senescence. The results indicated no definitive pattern of acceleration in leaf senescence with increasing salt stress. Salt regulation was also unaffected as leaves aged under increasing NaCl concentrations. The results are consistent with those of previous studies of the halophyte which indicated that the species was very tolerant of high NaCl concentrations.     

Age,smoking habits,heat stress,and their interactive effects with carbon monoxide and peroxyacetylnitrate on man's aerobic power

Metabolic, body temperature, and cardiorespiratory responses of 16 healthy middle-aged (40–57 years) men, 9 nonsmokers and 7 smokers, were obtained during tests of maximal aerobic power at ambient environmental temperatures of 25 ± 0.5 and 35 ± 0.5°C and 20% relative humidity under four conditions: (a) filtered air, FA; (b) 50 ppm carbon monoxide in filtered air, CO; (c) 0.27 ppm peroxyacetylnitrate in filtered air, PAN; and (d) a combination of all three mixtures, PANCO. There was no significant change in maximum aerobic power \(\left( {\dot VO2max} \right)\) related to the presence of air pollutants, although total working time was lowered in the 25°C environment while breathing CO. Older nonsmokers did have a decrement in \(\left( {\dot VO2max} \right)\) while breathing 50 ppm CO, while older smokers failed to show any change. This difference was related to the initial COHb levels of the smokers, who, when breathing this level of ambient CO, had only a 14% increase in COHb over their initial levels in contrast to the 200% increase in the nonsmokers. Smoking habits were the most influential factor affecting the cardiorespiratory responses of these older men to maximal exercise. Regardless of ambient conditions, smokers had a significantly lower (27%) aerobic power than nonsmokers, were breathing closer to their maximal breathing capacities throughout the walk, and had a higher respiratory exchange ratio. While the \(\left( {\dot VO2max} \right)\) of nonsmokers was only 6% less than that of younger nonsmoking males ( \(\bar x\) age = 25 years) working under similar conditions, the aerobic power of the older smokers was 26% lower than that of young smokers ( \(\bar x\) age = 24 years).