Stabilization of Z-DNA by demethylation of thymine bases: 1.3-A single-crystal structure of d(m5CGUAm5CG)

Methylation of cytosine bases at the C5 position has been known to stabilize Z-DNA. We had previously predicted from calculations of solvent-accessible surfaces that the methyl group at the same position of thymine has a destabilizing effect on Z-DNA. In the current studies, the sequence d(m5CGUAm5CG) has been crystallized and its structure solved as Z-DNA to 1.3-A resolution. A well-defined octahedral hexaaquomagnesium complex was observed to bridge the O4 oxygens of the adjacent uridine bases at the major groove surface, and four well-structured water molecules were found in the minor groove crevice at the d(UA) dinucleotide. These solvent interactions were not observed in the previously published Z-DNA structure of the analogous d(m5CGTAm5CG) sequence. A comparison of the thymine and uridine structures supports our prediction that demethylation of thymine bases helps to stabilize Z-DNA. A comparison of this d(UA)-containing Z-DNA structure with the analogous d(TA) structure shows that access of the O4 position is hindered by the C5 methyl of thymine due to steric and hydrophobic inhibition. In the absence of the methyl group, a magnesium-water complex binds to and slightly affects the structure of the Z-DNA major groove surface. This perturbation of the solvent structure at the major groove surface is translated into a much larger 1.41-A widening of the minor groove crevice, thereby allowing the specific binding of two water molecules at well-defined sites of each internal d(UA) base pair. Possible mechanisms by which modifications at the major groove surface of Z-DNA can affect the solvent properties of the minor groove crevice are discussed.     

Rate of acclimation of the tropical salt-marsh fish Cyprinodon dearborni to temperature changes

The acclimation rates of temperature changes in Cyprinodon dearborni, collected from Laguna Los Patos, Cumana, Venezuela, were determined by the critical thermal maximum method. At an increase in temperature (from 24 to 31°C) fish started to gain acclimation level after 3 hours and took 3 days to fully get up to a higher level of resistance to heat death; however, at a decrease in temperature (from 3 t to 24°C) fish began to lose its acclimation level after 12 days and required 39 days to reach a lower level of resistance to thermal death.     

Regulation of proton leakage from broken chloroplasts by CF0.

Measurements of proton translocation in CF₁-depleted, N, N′-dicyclohexylcarbodiimide-resealed broken chloroplasts were made under different light intensities. Kinetic analysis of the data shows that the outward leakage of accumulated protons through CF₀ is still dependent on light intensity with a first-order rate constant equal to mR₀, where R₀ is the initial rate of proton uptake which normally increases with light intensity and m is a characteristic constant which is independent of proton gradient and light intensity. Measurements of proton translocation in these modified chloroplasts cross-linked with glutaraldehyde under illumination and in the dark respectively suggest that the light-dependent proton leakage through CF₀ is regulated by conformation change in the membrane. It is proposed that the ovserved regulation of proton leakage through the CF₁.CF₀ complex in native chloroplasts is for optimizing the steady state synthesis of ATP under different light intensities.     

Treatment of Taenia saginata infection with mixture of areca nuts and pumpkin seeds.

In January and February 1974, 32 adults (20 males and 12 females) and a 13-year-old girl with taeniasis saginata were treated with the mixture of boiled areca nuts and pumpkin seeds at Mastoban, Jen-ai District, Nantou County, Taiwan. A total of 48 worms including 42 scolices were recovered from 29 cases. Side-effects were observed in 4 cases including 3 with complaints of dizziness, tinnitus, nausea and vomiting, and one with coma and abdominal pain. Mixtures of 75-150 g areca nuts and 50-100 g pumpkin seeds were judged effective and safe.     

The discrimination of nine different types of synaptic boutons in the fundus striati (nucleus accumbens septi)

An attempt has been made to discriminate additional types of synapses than have been previously described in the nucleus accumbens septi of the cat, which can, according to Brockhaus (1942), justifiably be termed the fundus striati due to the fact that it possesses all of the morphological and some of the neurochemical features of the striatum. This was undertaken in order to correlate at least one type of synapse with each different afferent pathway. Nine distinct types of synapses could be differentiated electron microscopically: Type I: axo-spinous synapses with sparse, small, round vesicles which seemed to be the nigro-striatal endings (35%). Type II: axo-somatic or axo-dendritic en passant synapses containing small, round vesicles (3%). Type III: axo-spinous synapses filled with densely-packed, small, round vesicles displaying strong postsynaptic thickenings which seem to be cortico-striatal (17%). Type IV: large axo-spinous synapses with densely-arranged, small, round vesicles contacting larger spines branching off a pedicle (9%). Type V: axo-somatic or axo-dendritic synapses containing large pleomorphic vesicles, probably axon collaterals (1%). Type VI: axo-somatic or axo-dendritic synapses with elongated small vesicles (20 X 45 nm) (3%). Type VII: large axo-somatic or axo-dendritic synapses filled by densely-packed, small, round vesicles (11%). Type VIII: large axo-somatic or axo-dendritic synapses containing loosely-arranged, small, round vesicles (8%). Type IX: axo-somatic or axo-dendritic synapses containing large, round vesicles in a translucent axoplasm (13%).     

Experimental studies on a lethal gene (1) in the Mexican axolotl, Ambystoma mexicanum.

1. Gene ? is a recessive lethal factor found in the white strain of axolotls. Animals heterozygous for the gene are phenotypically normal. When mated with each other they give offspring 25% of which exhibit the lethal effects of the gene. 2. The ?/? homozygotes develop normally to an advanced embryonic stage (Harrison stage 40) before the effects of the gene are first manifested. They then come to display a characteristic combination of abnormalities, including a disproportionately small head, small and poorly developed eyes, abnormal poorly developed gills, undifferentiated limb buds, and reduced overall growth rate. They may feed briefly, but soon stop and invariably die within a few weeks of the time of hatching. 3. The action of gene ? has been analyzed by parabiosing mutant and normal embryos, and by grafting various organ primordia reciprocally between mutant and normal embryos. Parabiosis to normal embryos fails to correct the abnormalities of the mutants, although their survival may be somewhat prolonged. Grafts of mutant organ primordia (eye, limb, gill, pronephros, gonad, head) also invariably fail to show improved development or to survive on normal hosts; normal organ primordia develop normally on mutant hosts so long as the mutant survives. These experiments indicate that gene ? is a recessive autonomous cell lethal affecting all of the organ systems during late embryonic and early larval development.