Proteolysis in quaking mouse brain and spinal cord

Six proteolytic enzymes were assayed for activity in quaking CNS in examining the hypothesis that increased proteolytic activity contributes to the hypomyelination characteristic of this mutant. Cathepsin B-like enzyme, cathepsin D, neutral proteinase, calcium-activated neutral proteinase, prolyl endopeptidase, and diaminopeptidase II were assayed in whole homogenate of brain or spinal cord and each was found to have activity similar to that in normal mice. These results do not support a relationship between proteolysis and the genetic defect and suggest that other factors should be investigated to delineate the pathogenesis of this mutant.     

Resistance of wild wheat to stripe rust: Predictive method by ecology and allozyme genotypes

From 114 accessions of wild emmer wheat from 11 sites in Israel, known for their allozymic variation (Nevo & al. 1982), individual genotypes were tested for resistance to one isolate of stripe rust both in the seedling stage in a growth chamber and in the adult plant stage in the field. The results indicate that resistance to stripe rust in seedlings and adults are significantly correlated (r_s = 0.40, p < 0.001). Genetic polymorphisms of resistance to stripe rust vary geographically and are predictable by climatic, as well as allozymic markers. Three variable combinations of rainfall, evaporation, and temperature explain significantly 0.40–0.53 of the spatial variance in disease resistance to stripe rust, suggesting the operation of natural selection. Several allozyme genotypes are significantly associated with disease resistance. We conclude that natural populations of wild emmer wheat in Israel contain large amounts of disease resistance genes. These populations could be effectively screened and then utilized by the phytopathologist for identifying resistant genotypes and producing new resistant cultivars.Patterns of Resistance of Wild Wheat to Pathogens in Israel II.     

Larvae of Euphausia superba in the Scotia Sea and Bransfield Strait in March 1984 — Development and abundance compared with 1981 larvae

Summary Larvae of Euphausia superba in the Atlantic sector of the Antarctic in March 1984 averaged 580 per 1000 m³ of water. This is 100 times less than we observed in March 1981, but more than the average of 250 larvae per 1000 m³ found in January–February 1981. There was one 1984 high-abundance sample, accounting for 85% of all larvae caught, from the eastern area of confluence of Drake Passage and Weddell Sea waters. Abundances in 1984 near the South Shetland Islands were commonly 5 to 10 larvae per 1000 m³, and younger by 2 to 4 developmental stages than in March 1981. Body lengths of given stages were generally less in 1984 than in 1981. Advanced furcilia stages, particularly, in the 1984 samples tended to be smaller than the same stages in March 1981, indicating relatively poor growth during February 1984. However, the 1984 younger larvae (calyptopes and the developmental forms of furcilia stages 1 and 2) indicated that, in 1984, recent (March) growth had been good — probably better than in February. Dierct observation of the development of calyptopis stage 3 to furcilia stage yielded a development time of 7.7 days, which compares favorably to the 8-day period estimated from field samples. Reduced food availability did not affect the development rate nor give rise to a clearly higher incidence of indirect pathways of development. It is postulated that recruitment was about of month later in 1984 than in 1981 in most of the area studied and was probably going to be less successful.     

Structural requirements for anion substrates of the methotrexate transport system in L1210 cells

A broad spectrum of structurally diverse anions reversibly inhibits the influx of methotrexate in L1210 cells. Several of the more effective anions and their respective inhibition constants (K_i values) were: 5-methyltetrahydrofolate (0.3 μm), bromosulfophthalein (2 μm), thiamine pyrophosphate (3 μm), 8-anilino-1-naphthalene sulfonate (7 μm), phthalate (20 μm), and AMP (50 μm). Moderate inhibition was observed with P_i (K_i = 400 μm) and other divalent inorganic anions, while small monovalent anions such as Cl^? (K_i = 30 mm) were the least effective. When these same anions were tested for an effect on methotrexate efflux, stimulation was observed with some anions, while others had no effect. Enhancement was produced by folate compounds and p-aminobenzoylglutamate, small monovalent (e.g., Cl^?, acetate, and lactate) and divalent (e.g., phosphate and succinate) anions, a few nucleotides (e.g., AMP), and thiamine pyrophosphate, while little or no effect was associated with trivalent anions (e.g., citrate), most nucleotides, and large organic anions (e.g., bromosulfophthalein, NAD, and NADP). Anions with the ability to promote methotrexate efflux in control cells lost this capacity upon exposure of the cells to an irreversible inhibitor of methotrexate influx. These results support the hypothesis that methotrexate transport proceeds via an anion-exchange mechanism and moreover provide evidence that anion substrates for this system can be identified by their ability to promote methotrexate efflux. Anions which appear most likely to participate in this exchange cycle in vivo are P_i and AMP.     

Complexes between mitochondrial enzymes and either citrate synthase or glutamate dehydrogenase

Experiments performed in polyethylene glycol and with a divalent crosslinker indicate that both mitochondrial malate dehydrogenase and aspartate aminotransferase can form hetero enzyme—enzyme complexes with either glutamate dehydrogenase or citrate synthase. In general, these as previous results indicate that complexes with the aminotransferase are favored over those with malate dehydrogenase and complexes with glutamate dehydrogenase are favored over those with citrate synthase. When the levels of enzymes are low, the only detectable complex is between the aminotransferase and glutamate dehydrogenase. Under these conditions, palmitoyl-CoA is required for complexes between the other three enzyme pairs, however, palmitoyl-CoA also enhances interactions between glutamate dehydrogenase and the aminotransferase. DPNH disrupts complexes with malate dehydrogenase and has little effect on those with the aminotransferase, while oxalacetate disrupts complexes with citrate synthase but has little effect on those with glutamate dehydrogenase. The citrate synthase-aminotransferase complex was favored in the presence of DPNH plus malate, which disrupt the other three enzyme-enzyme complexes. Glutamate dehydrogenase has a higher affinity and capacity than citrate synthase for palmitoyl-CoA. Consequently, lower levels of palmitoyl-CoA are required to enhance interactions with glutamate dehydrogenase. Furthermore, glutamate dehydrogenase can compete with citrate synthase for palmitoyl-CoA and thus can prevent palmitoyl-CoA from enhancing interactions between citrate synthase and either malate dehydrogenase or the aminotransferase.     

Mitogenic response to epidermal growth factor (EGF) modulated by platelet-derived growth factor in cultured fibroblasts

The mitotic effects of epidermal growth factor (EGF) were investigated in two cultured fibroblast lines, BALB/c-3T3 and C3H 10T1/2 cells. EGF (30 ng/ml) added to quiescent 3T3 cells in medium containing either platelet-poor plasma or 10(-5) M insulin caused only minimal increases in the percentage of cells stimulated to initiate DNA synthesis. In contrast, EGF acted synergistically with either insulin or plasma to stimulate DNA synthesis in quiescent cultures of 10T1/2 cells, although the maximum effects of EGF were measured at concentrations several-fold greater than those found in either serum or plasma. In either 3T3 or 10T1/2 cells a transient preexposure to platelet-derived growth factor (PDGF) caused over a 10-fold increase in the sensitivity to the mitogenic effects of EGF. It is therefore possible that a primary action of PDGF is to increase the sensitivity of fibroblasts to EGF, independent of whether EGF alone is found to be mitogenic.     

Paleolimnology of the Peten Lake District,Guatemala

Long-term changes of sedimentary particle-size distribution in two tropical lowland lakes were compared with changes of human population sizes, estimated archaeologically, in the drainage basins. Mean particle size of silt and clay fractions (<64 µm) varied between 3 and 15 µm. High positive skewness and kurtosis of the distributions were associated with smaller particle sizes; hence small mean size resulted from greater influx of small particles while influx of larger particles was probably constant. An inverse correlation between mean particle size and human population size is interpreted to mean that disturbance-induced erosion results in delivery of very fine inorganic particles at higher rates. Within any one basin, particle-size stratigraphy is more precisely related to archaeological time periods than is pollen stratigraphy. An absolute chronology still eludes us, owing to the failure of ¹⁴C dating of calcareous, colluvial sediments, but our relative chronology is now more precise than before. If certain assumptions about past hydrologic relations can be met, particle-size analysis is a way of comparing the histories of geographically very different lakes, including lakes from tropical, temperate, and arctic regions.     

Effect of parasympathetic denervation on acetylcholine levels in the rat parotid gland. Is there an extraneuronal pool of acetylcholine?

Parasympathetic denervation of the rat parotid gland by avulsion of the auriculotemporal nerve caused a marked and lasting decrease in gland weight. Parasympathectomy did not change the levels of choline in the gland but decreased by 60% the levels of acetylcholine (ACh) ten days after surgery and 65% at 28 days. It is puzzling that relatively high levels of ACh remained after parasympathetic denervation. The presence of additional cholinergic nerves that innervate the gland, or pass through it en route to other structures may account for some of the remaining ACh. Also, Schwann cells from denervated nerves might have contributed to some of the ACh. The existence of an extraneuronal source of ACh is considered.