Involvement of voltage-dependent calcium channels (VDCC) in the action of GnRH on GtH release in common carp (Cyprinus carpio L): comparison with K+ action.

The involvement of different types of voltage-dependent calcium channels (VDCC) in the stimulatory action of GnRH (in comparison with K+) on maturational gonadotropin (GtH) release was investigated using superfused carp pituitary cells. The action of these 2 stimulants was not modified either by D600 or nifedipine (drugs blocking L-type of VDCC). Cadmium (Cd2+), which blocks all types of VDCC indifferently, provoked a dose-dependent stimulation of GtH secretion. Cd2+ action was not altered by addition of sGnRH in any of the doses. Similar results were obtained using K+ as a secretagogue, but only the highest dose of Cd2+ (200 mumol/l) was able to completely block K+ action. Low doses (0.1 and 1 mumol/l) of the L-type VDCC activator BAY-K8644 did not change basal GtH secretion and had no effect on sGnRH-stimulated GtH secretion. Surprisingly, doses (10 mumol/l and higher) of BAY-K8644 evoked dose-dependent inhibition of GtH secretion. On the other hand, a higher concentration (20 mumol/l) of nifedipine provoked a stimulation of GtH release. Our results indicate that the stimulatory action of GnRH and K+ involves activation of a certain type of cadmium-sensitive VDCC (probably T- or N-type VDCC) whereas dihydropyridine and diphenylalkylamine sensitive VDCC (L-type VDCC) does not participate in this phenomenon. The inhibitory action of BAY-K8644 and, on the other hand, the stimulatory action of nifedipine indicate that L-type VDCC probably play a role in other physiological pathways regulating GtH release in carp.     

Circadian rhythms in Neurospora crassa: the effects of point mutations on the proteolipid portion of the mitochondrial ATP synthetase

Summary Five oligomycin-resistant (oli ^r) mutant strains of Neurospora crassa were analyzed for their growth rate and for the periodicity of their circadian rhythm. The most resistant strains had periods of 18–19 h while the least resistant strain had a normal period of 21.0 h. There was a rough correlation between the in vivo degree of oligomycinresistance and the amount of change in the period. Several of the oli ^r mutations have been previously described by Sebald et al. (1977) in terms of known amino acid changes in the primary structure of the proteolipid, or DCCD-binding protein, found in the F₀ membrane portion of the mitochondrial ATP synthetase. Amino acid changes in the structure of this protein are reported here for two other oli ^r mutations. The proteolipid isolation procedures were slightly modified to include a delipidation step, and an HPLC procedure was developed to separate the hydrophobic peptides of this protein. Analysis of heterocaryons carrying both the oli ^r and oli ^s markers indicated that the oli ^r and oli ^s mutations were codominant to each other in terms of period and growth rate. The changes in the primary structure of this DCCD-binding protein reported here are the first known examples of changes in the primary structure of a protein which alter the period of a circadian rhythm.     

The fate of newly made DNA in Escherichia coli mutants thermosensitive in DNA synthesis

Summary E. coli mutants exist in which DNA synthesis is thermosensitive. In one class of these mutants DNA synthesis stops immediately if a critical temperature (42°C) is reached. When DNA replication in such mutants is followed by ³H thymidine incorporation at 33°C, it is found that 1. only the newly made DNA is degraded at 42°C, 2. the discontinuously replicated DNA is lost predominantly at 42°C, 3. 1–3% of the chromosomal DNA is rendered acid soluble at 42°C without concomitant loss of viability of the cells at 33°C.Replication of phage DNA is inhibited in the same mutant at 42°C. However, when DNA synthesis is followed in infected cells at 33°C it is found that 1. no degradation of specific DNA seems to occur at 42°C in the early phase of infection, 2. replicating DNA molecules in the late phase of infection are completed at 42°C before DNA synthesis comes to a halt.     

Stabilization by ATP and ADP of Escherichia coli dnaB protein activity

The effect of adenine ribonucleotides on the stability of Escherichia coli dnaB protein in cellular crude extracts was studied. Stabilization of dnaB protein by ATP or ADP, but not by AMP, was manifested in that (i) the activity and yield of wild type dnaB protein is enhanced in the presence of ATP, (ii) the dnaB protein of E. coli dnaB mutants, such as groPB and dnaB252/ColE1::dnaC+, which is inactive in a dnaB complementation assay, can be isolated in active form in the presence of ATP or aDP, (iii) ATP or ADP protect the dnaB protein of an E. coli dnaBts mutant from inactivation at 37 degrees C, and (iv) inactive groPB and dnaBts protein can be reactivated partially by ATP. Thus, the stabilizing effect of ATP and ADP can be exploited for the isolated of otherwise inactive or labile mutant dnaB proteins.     

Revisiting the use of Iprodione and Trichoderma in the integrated management of onion white rot

The biocontrol properties of Trichoderma species are well documented, but their effectiveness in antagonism of the problematic Sclerotium cepivorum, the causal agent of white rot in Allium species, appears limited with reports of significant control only relating to deliberately-mutated strains of Trichoderma. Our previous studies have indicated the possibility of using selected naturally-occurring strains of the antagonist in the suppression of other diseases; now in vitro and controlled environment in vivo studies have indicated that a degree of control of Onion White Rot is possible, and that the selected antagonist strains can be used in integrated treatments with Iprodione to good effect. The possible value of such treatments is considered in light of other approaches to the suppression of this continuing problem.     

Proteus syndrome: a case with clonal chromosome aberration

Proteus syndrome is a disorder characterized by overgrowth of multiple tissues, connective tissue nevi, epidermal nevi and hyperostoses with asymmetric involvement. The clinical expression of the disorder is extremely variable. Molecular pathogenesis of the syndrome is unknown but it is hypothesized that it resulted from a somatic alteration of a gene leading to mosaic effects that would be lethal if the mutation was carried in nonmosaic fashion, and this may explain the variability among patients. We report a new case who presented at birth with asymmetric hypertrophy of the bones and soft tissues of fingers and a tumor of the chest. Cytogenetic analysis of the excised tumor revealed clonal chromosome aberration: mos46, XY, add(9)(p13) [5]/46,XY[30]. During follow up tumors of the rectum and urinary bladder were diagnosed.