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Biomedical subjects

D H Hall

Publications and source records attributed to D H Hall.

At least 55 records · Page 3Linked to original sources
PubMed1988

Satellite glial cells penetrate neurosecretory cells to perinuclear position in the goldfish preoptic area.

Some goldfish neurosecretory cells have plasma membrane invaginations filled by processes of surrounding satellite glial cells (SCs) that produce trophospongium-like multicellular neuron-glial aggregates. Some penetrating SC processes approach the neuronal nucleus, reaching to within approximately 40 nm of the outer nuclear membrane. Gap junctions were found in one freeze-fracture replica through an apparent neuronal-glial aggregate, suggesting that neuron-glial gap junctions may be present. The extensive covering and penetration of these neurons by SCs suggests trophic relationships and communication by undetermined modalities between neurons and glia. The common close proximity of invaginated SC processes to the neuronal nucleus may indicate that information is transmitted between SCs and the nucleus. Some SCs abut against the basal lamina of large blood vessels and contain dense vesicles, either secretory or lysosomal.

Animals↗
PubMed1988

Neuronal and glial gap junctions in the goldfish preoptic area, a thin section and freeze-fracture study.

In freeze-fracture, both large macular gap junctions and long thin gap junctions surrounded by a strand of tight junction were found on neurosecretory cells. Preoptic neurons show large areas of soma-to-soma apposition, but thin section showed no evidence for gap junctions between neuronal somata. Neurosecretory cell neurites formed parallel bundles in neuropil lateral to the nucleus, and gap junctions were found between the neurites. These junctions apparently correspond to macular junctions seen on neurosecretory elements in freeze-fracture. Some large macular gap junctions found in freeze-fracture presumably correspond to junctions seen between glial cells in thin section. However, glial membranes lacked characteristics distinguishing them from neuronal membranes. In one instance, a large apparent glial sheet process formed both macular and long thin gap junctions on different surfaces. The long thin gap junctions that were surrounded by a strand of tight junction were formed with a large neurosecretory cell soma. Extensive pinocytosis was observed at some membranes forming gap junctions.

Animals↗
PubMed1988

The elasmobranch spiracular organ. I. Morphological studies.

The spiracular organ is a lateral line derived receptor associated with the first gill cleft (spiracle). Its functional morphology was studied in the little skate, Raja erinacea, and a shark, the smooth dogfish, Mustelus canis, with light and electron microscopy. The spiracular organ is a tube (skate) or pouch (shark) with a single pore opening into the spiracle. The lumen is lined with patches of sensory hair cells, and filled with a gelatinous cupula. In the little skate, hair cells form synapses with afferents but apparently not with efferent fibers. In both species, the spiracular organs are deformed by flexion of the hyomandibular cartilage at its articulation with the cranium. The hyomandibula is a suspensory element of the jaws; hyomandibular flexion results in jaw protrusion. The little skate spiracular organ is anchored at one end to the cranium and at the other to the hyomandibula so that it is stretched or relaxed during hyomandibular extension and flexion, respectively. In Mustelus, the effects of hyomandibular flexion on the spiracular organ are mediated indirectly by the superior post-spiracular ligament which inserts on the distal end of the hyomandibula. Deformation of the dogfish shark cupula during hyomandibular movement was observed. In the little skate, as revealed by transmission electron microscopy, there is a measurable deflection of the hair cell ciliary bundles from spiracular organs fixed with the hyomandibula in the flexed relative to the extended positions. In both species, hyomandibula flexion should result in hair cell depolarization, and sensory afferent excitation, based on the direction of the observed (skate) or expected (shark) deflection of hair cell cilia.

Animals↗
PubMed1987

Two domains for splicing in the intron of the phage T4 thymidylate synthase (td) gene established by nondirected mutagenesis.

Of 97 nondirected T4 thymidylate synthase-defective (td) mutations, 27 were mapped to the intron of the split td gene. Clustering of these intron mutations defined two domains that are functional in splicing, each within approximately 220 residues of the respective splice sites. Two selected mutations, tdN57 and tdN47, fell within phylogenetically conserved pairings, with tdN57 disrupting the exon I-internal guide pairing (P1) in the 5' domain and tdN47 destabilizing the P9 helix in the 3' domain. A splicing assay with synthetic oligonucleotides complementary to RNA junction sequences revealed processing defects for T4tdN57 and T4tdN47, both of which are impaired in cleavage at the 5' and 3' splice sites. Thus prokaryotic genetics facilitates association of specific residue changes with their consequences to splicing.

Base Sequence↗
PubMed1987

Genetics of cell and axon migrations in Caenorhabditis elegans.

The Caenorhabditis elegans epidermis comprises 78 cells which cover the external surface of the embryo as a single cell layer. These cells secrete the cuticle from their exterior faces and support the body wall muscles and most of the nervous system on their interior faces. The epidermal cells arise by autonomous embryonic cell lineages but show regulative interactions after their assembly into an epithelium. It is believed that the various epidermal cells express different kinds or amounts of surface molecules that govern their mutual assembly and also guide the attachments and migrations of the underlying body muscles and neurones. The first muscles and neurones may in turn express new surface molecules that refine later cell movements. Mutations in some 30 known genes disrupt the movements of cells or axons along the body wall.

Animals↗
PubMed1986

The giant fiber and pectoral fin adductor motoneuron system in the hatchetfish.

In the medulla of the hatchetfish each Mauthner fiber forms chemical synapses on a number of large myelinated axons termed giant fibers. The giant fibers form rectifying electrotonic synapses on pectoral fin adductor motoneurons, and in this fish bilateral pectoral fin adduction is an important component of the Mauthner fiber-mediated escape reflex. The branching patterns of giant fibers were determined by intracellular injection of Lucifer yellow. Dye coupling to the motoneuron somata was not observed, although a low level of transfer might have been obscured by autofluorescence. Individual giant fibers terminate primarily on pectoral fin motoneurons contralateral to their cell bodies, but may also send a branch back across the midline to ipsilateral motoneurons. The rostral process of each giant fiber ends on neurons presumably associated with cranial musculature. The number and geometry of the pectoral fin motoneurons were determined using Golgi and Nissl staining and serial reconstruction methods.

Animals↗
PubMed1985

Ultrastructure of the rectifying electrotonic synapses between giant fibres and pectoral fin adductor motor neurons in the hatchetfish.

Synapses formed by giant fibres on pectoral fin adductor motor neurons were identified by horseradish peroxidase (HRP) injection. The synapses were distributed in clusters on the somata and proximal dendrites of the motor neurons. All of the labelled synapses contained synaptic vesicles and often had clearly defined active zones characteristic of chemical synapses. Some synapses also showed gap junctions with the motor neuron soma, often directly adjacent to an active zone. The gap junctions were asymmetrical, with a thick layer of electron dense material on the postsynaptic side. Previous electrophysiological data indicate that giant fibre inputs to motor neurons are purely electrotonic and that these electrical synapses rectify.

Action Potentials↗
PubMed1984

Genetic evidence for physical interactions between enzymes of nucleotide synthesis and proteins involved in DNA replication in bacteriophage T4.

We have found that mutations in phage T4 genes 41 (five of five) and 61 (three of three) cause resistance to the folate analogue pyrimethamine that inhibits T4 dihydrofolate (FH2) reductase. These genes code for subunits of a T4 primase and are part of a putative T4 replication complex. In contrast to many previously isolated folate analogue-resistant (Far) T4 mutants, these T4 primase mutants do not overproduce FH2 reductase nor do they alter its primary structure. A new mutant with a single lesion in gene 41 was isolated which proved resistant to the folate analogue at 30 degrees and was lethal at 42 degrees. This mutant induced normal levels of FH2 reductase (encoded by the frd gene) and appeared to have normal expression of other T4 genes at 30 degrees. Like other mutations in gene 41, tsP129 reduced phage-induced DNA synthesis to about 15% that of wild-type T4 as measured by thymidine incorporation under restrictive conditions. Double mutants carrying mutations in genes 41 and 61, 41 and frd or 61 and frd showed allele-specific suppression suggesting that the products of these genes interact. We suggest that abnormal interactions between components of the replication complex and a DNA precursor synthesizing complex cause folate analog resistance by allosterically altering the T4 FH2 reductase.

Chromosome Mapping↗
PubMed1984

Physical mapping and complete nucleotide sequence of the denV gene of bacteriophage T4.

Phage T4 deletion mutants that are folate analog resistant (far) and contain deletions in the region of the T4 genome near denV have been isolated previously. We showed that one of these mutants (T4farP12) expressed normal denV gene activity, whereas another mutant (T4farP13) was defective in the denV gene. The rII-distal (right) physical endpoints of these deletions defined the limits of the interval in which the rII-proximal (left) endpoint of the denV gene should be located. The deletion endpoints were identified by restriction and Southern hybridization analyses of phage derivatives containing deoxycytidine instead of hydroxymethyldeoxycytidine in their DNAs. The results of these analyses localized the rII-proximal (left) end of the denV gene to a region between 62.4 and 64.3 kilobases on the T4 physical map. denV+ phage resulted from marker rescue with two of five denV- alleles tested, using plasmids containing a 1.8-kilobase fragment from this region or a 179-base-pair terminal fragment derived from it. Sequencing of the 179-base-pair fragment from wild-type DNA showed a 130-base-pair open reading frame with its termination codon at the rII-proximal end. Confirmation that this open reading frame is part of the denV coding sequence was obtained by identifying a TAG amber codon in the homologous DNA derived from a denV amber mutant strain. This mutant strain rescued the denV+ allele from plasmids containing the wild-type sequence. An adjacent overlapping restriction fragment was also cloned, permitting determination of the remaining denV gene sequence. Based on these results, the 3' end of the coding region of the denV locus was mapped to kilobase position 64.07 on the T4 physical map, and the 5' end was mapped to position 64.48.

Base Sequence↗
PubMed1983

Gap junctions and septate-like junctions between neurons of the opisthobranch mollusc Navanax inermis.

The buccal ganglia of Navanax inermis were studied by thin section, lanthanum infiltration and freeze fracture. Freeze fracture clearly demonstrates small gap junctions between neuronal processes in the neuropil, many of which are known to be electrotonically coupled. Junctional particles cleave with the P-face. In thin section, gap junctions appeared as small blurred contacts, presumably because of the small size of the junctions. Lanthanum infiltration was poor and failed to aid in identifying gap junctions. However, it did reveal septate-like junctions whose septa were not osmiophilic. Corresponding E-face grooves and ridges were seen in freeze fracture, sometimes adjacent to gap junctions. The septate-like junctions have parallel membranes and may have been mistaken for gap junctions in several other thin section studies of invertebrate neurons.

Animals↗
PubMed1983

alpha-Bungarotoxin labeling and acetylcholinesterase localization at the Mauthner fiber giant synapse in the hatchetfish.

Autoradiographic and histochemical techniques have been used to characterize further the pharmacology of transmission at the Mauthner fiber giant synapse of the South American hatchetfish. [125I]alpha-Bungarotoxin was applied to hatchetfish medullae and a standard autoradiographic procedure was carried out on 3- to 4-microns sections of glutaraldehyde-fixed tissue. All Mauthner fiber giant synapses, as identified by light microscopic criteria, had closely associated silver grains. Labeling was blocked by d-tubocurarine. Glutaraldehyde-fixed slices of hatchetfish medulla were stained histochemically for acetylcholinesterase; all giant synapses that could be identified in the light microscope showed heavy deposits of reaction product. Staining was blocked by diisopropyl-fluorophosphate, which inhibits both pseudocholinesterase and acetylcholinesterase, but was not blocked by tetraisopropylpyrophosphoramide, a specific pseudocholinesterase inhibitor. This evidence strongly supports the suggestion that the Mauthner fiber giant synapse is nicotinic cholinergic.

Acetylcholinesterase↗
PubMed1981

Suppressors of mutations in the rII gene of bacteriophage T4 affect promoter utilization.

Homyk, Rodriguez and Weil (1976) have described T4 mutants, called sip, that partially suppress the inability of T4rII mutants to grow in lambda lysogens. We have found that mutants sip1 and sip2 are resistant to folate analogs and overproduce FH2 reductase. The results of recombination and complementation studies indicate that sip mutations are in the mot gene. Like other mot mutations (Mattson, Richardson and Goodin 1974; Chace and Hall 1975; Sauerbier, Hercules and Hall 1976), the sip2 mutation affects the expression of many genes and appears to affect promoter utilization. The mot gene function is not required for T4 growth on most hosts, but we have found that it is required for good growth on E. coli CTr5X. Homyk, Rodriguez and Weil (1976) also described L mutations that reverse the effects of sip mutations. L2 decreases the folate analog resistant and the inability of sip2 to grow on CTr5X. L2 itself is partially resistant to a folate analog, and appears to reverse the effects of sip2 on gene expression. These results suggest that L2 affects another regulatory gene related to the mot gene.

Gene Expression Regulation↗
PubMed1981

Acute ethylene oxide intoxication.

A case of acute ethylene oxide intoxication is described in which neurological involvement was present. Three recurrent seizures over a period of an hour were observed in a 43-year-old female. The patient continued to complain of malaise and inability to perform minor motor tasks up to one week after discharge. Neurological evaluation conducted three weeks after toxic exposure was completely normal. A two-month follow-up showed the patient to be asymptomatic without recurrence of symptoms.

Acute Disease↗
PubMed1980

Modulation of cyclic AMP-dependent protein kinase by vasopressin and calcitonin in cultured porcine renal LLC-PK1 cells.

We have previously demonstrated that a cultured porcine kidney cell, LLC-PK(1), maintains the characteristics of a polar renal epithelial cell in culture, and responds to salmon calcitonin and [arginine]vasopressin by increasing cyclic AMP content. To demonstrate the usefulness of this cell line as a model for the study of the biochemical events distal to cyclic AMP production, the activation of cyclic AMP-dependent protein kinase was examined. Intact cells in monolayer demonstrated progressive increases in cyclic AMP content and activation of protein kinase in response to [arginine]vasopressin (2-200nm) and salmon calcitonin (0.03-30nm) with both hormones fully activating the enzyme at a cell cyclic AMP content of 35pmol/mg of protein. Of the total cyclic AMP-dependent protein kinase activity, 80% was found in the 27000g supernatant fraction of sonicated cell material, and this soluble protein kinase could be fully activated by hormone. Conversely, the 27000g pellet contained a significant proportion of cyclic AMP-independent protein kinase and only 20% of total cell cyclic AMP-dependent protein kinase; the latter showed little response to hormone. On the basis of DEAE-cellulose chromatography, type II protein kinase was the predominant isoenzyme in both soluble and particulate fractions of the LLC-PK(1) cells and the soluble fractions of rat and guinea-pig renal medulla. Thus, the LLC-PK(1) cell line can serve as a model for hormonal modulation of protein kinase and as a potential source for defining the endogenous substrates for these enzymes.

Animals↗
PubMed1980

Suppressors of mutations in the bacteriophage T4 gene coding for both RNA ligase and tail fiber attachment activities.

The protein product of T4 gene 63 catalyzes both the attachment of tail fibers to fiberless phage particles and the ligation of single-stranded RNA (Snopek at al., Proc. Natl. Acad. Sci. U.S.A. 74:3355-3359, 1977). To investigate whether the gene 63 product has a role in nucleotide metabolism, we isolated false revertants of amM69 in gene 63. We screened for revertants that could grow at 30 degrees C but not at 43 degrees C on Escherichia coli OK305 when nucleotides were limiting. These false revertants contained the original mutation in gene 63 and new suppressor mutations. Some of these suppressor mutations caused temperature sensitivity by themselves, allowing single mutants carrying the suppressor to be recognized and isolated. The results of mapping and complementation studies indicated that most of these ts suppressors were in the t gene (lysis), one was in gene 5 (baseplate), and one was in gene 18 (sheath). The mutation in gene 18, tsDH638, suppressed three different amber mutations in gene 63 but did not suppress amber mutations in several other genes. None of the suppressors that were characterized were in genes with known functions in nucleotide metabolism. However, an intriguing property of these false revertants was that they were very sensitive to hydroxyurea, an inhibitor of nucleotide metabolism.

Chromosome Mapping↗
PubMed1976

Novel mechanism of resistance to folate analogues: ribonucleoside diphosphate reductase deficiency in bacteriophage T4.

Some spontaneously occurring bacteriophage T4 mutants (far mutants) were able to form plaques in the presence of concentrations of folate analogues that completely inhibit plaque formation by wild-type phage T4. Some of these far mutants were shown to be ribonucleoside diphosphate (RDP) reductase (EC 1.17.4.1) deficient, and some independently isolated RDP reductase-deficient mutants (nrd mutants) were shown to be folate analogue resistant. The map positions of the RDP reductase-deficient far mutants were shown to be within the genes controlling the phage-induced RDP reductase activity.

Chromosome Mapping↗
PubMed1976

Utilization of early promotors in mutant far P85 of bacteriophage T4.

We show that farP85 is a recessive mutant of T4 incapable of activating the delayed early promotors for genes 43 and 45 and that the farP85 mutation is in the same complementation group as the ts G1 mutation, which is located in the "modifier of transcription" (mot) gene.

Coliphages↗