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C R Bailey

Publications and source records attributed to C R Bailey.

32 records · Page 2Linked to original sources
PubMed1980

A possible rôle for acid phosphatase in gamma-amino-n-butyrate uptake in Aspergillus nidulans.

Previously published work from another laboratory has shown that the mutation pacC-5 in the ascomycete Aspergillus nidulans leads to loss of an acid phosphatase (EC 3.1.3.2) activity and is probably located in the structural gene for this enzyme. Here, we show that, pleiotropically, pacC-5 considerably reduces gamma-amino-n-butyrate transport levels as shown both by direct uptake measurements and two kinds of growth tests. A reduction in expression of the permease specified by the gabA gene is almost certainly responsible for the gamma-amino-n-butyrate uptake defect in pacC-5 strains. pacC-5 does not reduce L-proline uptake, mainly mediated by the prnB permease, or beta-alanine uptake. This work and our previously published results suggest that, although it does not uniquely reduce gamma-amino-n-butyrate uptake, pacC-5 is highly selective in its effects on transport processes. It is therefore probable that the acid phosphatase specified by the pacC gene plays some rôle in the synthesis, membrane integration or functioning of a particular class of permeases. A rôle for acid phosphatases in membrane processes casts an intriguing new light on the fact that these enzymes are periplasmic and extracellular in many micro-organisms including A. nidulans.

Acid Phosphatase↗
PubMed1980

Genetic evidence for a second asparaginase in Aspergillus nidulans.

The apnA1 mutation strongly reduces L-asparagine utilization in Aspergillus nidulans. The ahrA1 mutation, leading to loss of an L-asparaginase (Drainas et al., 1977), eliminates residual L-asparagine utilization in double mutant strains also carrying apnA1. This additivity suggests that A. nidulans, like Saccharomyces cerevisiae (Jones, 1977; Dunlop et al., 1978), has two L-asparaginases specified by apnA and Ahr A, respectively, apnA has been mapped to a position on the left arm of linkage group II, in the sequence adH--acrA--apnA--wA--methA--palcA--(centromere).

Asparaginase↗
PubMed1979

Do the tightly linked structural genes for nitrate and nitrite reductases in Aspergillus nidulans form an operon? Evidence from an insertional translocation which separates them.

Previous work (Rand and Arst, 1977) led to the proposal that the nis-5 mutation results in a new low activity promoter for niiA, the structural gene for nitrite reductase in Aspergillus nidulans. Expression of niiA via this promoter differs from expression of niiA via its normal promoter/initiator in that expression by the new promoter is not subject to nitrate induction or ammonium repression. nis-5 reduces but does not abolish niiA expression mediated by the normal promoter/initiator. In this work we show that nis-5 is associated with and is probably identical to a non-reciprocal translocation in which a considerable portion of the centromere proximal region of the right arm of linkage group II is inserted into linkage group VIII between niiA and niaD, the tightly linked, probably contiguous structural genes for nitrate reductase. This implies that niiA, along with its normal promots yet unidentified by its normal role. Further, it indicates that niiA is transcribed from the niaD-proximal side. As niiA and niaD are separated by a large number of unrelated genes in nis-5 strains, we can safely conclude that expression of niiA does not occur solely by synthesis of a messenger which carries a niaD as well as a niiA transcript. Clearly, niiA and niaD do not form an operon for which a di- (or poly-) cistronic messenger by the only transcript. This is consistent with other experimental evidence which shows that the syntheses of nitrate and nitrite reductases are not coordinately regulated. Nevertheless, all of these data would also be consistent with a model in which niiA and niaD form an operon-type structure having overlapping transcripts, one being di- (or poly-) cistronic and including both niiA and niaD and another being monocistronic for niiA. The reduced niiA expression mediated by the normal promoter/initiator in nis-5 strains could be a consequence of the functioning or positioning of the new linkage group II niiA promoter. An alternative, but not mutually exclusive, explanation would be that the insertional translocation prevents synthesis of a niiA niaD dicistronic transcript so that only that component of niiA expression which is due to a monocistronic niiA messenger can be induced by nitrate (and nitrite) in nis-5 strains. The apparently low activity of the new linkage group II promoter in comparison to the normal niiA promoter/initiator might betoken considerable efficiency of the latter rather than any particular lack of efficiency of the former. In addition, this work has involved extensive new mapping in linkage group II, including both mitotic mapping of the centromere and meiotic mapping of previously unlocated markers. A series of crosses in cluding genotype combinations both heterozygous and homozygous for nis-5 has been used to map the break-points and orientation of the translocation. As one break-point is closer to the centromere of linkage group II than the most centromere proximal identified gene on the same (i.e...

Aspergillus nidulans↗
PubMed1979

Cis-dominant regulatory mutations affecting the expression of GABA permease in Aspergillus nidulans.

In Aspergillus nidulans expression of the gabA gene, the probable structural gene for the gamma-amino-n-butyrate (GABA) permease, is controlled by induction, via the intA gene, ammonium repression, mediated by the areA gene, and probably carbon catabolite repression. Regulatory mutations, tightly linked to gabA, were selected by reverting an areAr-2 strain on GABA as nitrogen source. These mutations, gabI-1, gabI-2, and gabI-3 result in increased gabA expression and are cis-dominant in their effects on the gabA gene. Mapping data show that the regulatory mutations map on one side of all gabA- alleles tested.

Aspergillus nidulans↗
PubMed1978

Lactam utilisation in Aspergillus nidulans: evidence for a fourth gene under the control of the integrator gene intA.

Mutations in the lamA gene of Aspergillus nidulans prevent the conversion of exogenous 2-pyrrolidone (gamma-butyrolactam) to gamma-amino-n-butyrate (GABA) and also prevent the (probably analogous) utilisation of 2-piperidone (sigma-valerolactam). The lamA gene, in linkage group VIII, probably specifies a lactamase but a rôle in lactam uptake cannot be ruled out. lamA is probably under the control of the positive acting regulatory gene intA, which can integrate its expression with the expression of three other genes, specifying acetamidase, GABA transaminase, and GABA permease, respectively.

Aspergillus nidulans↗
PubMedDate not supplied

Homology between Streptomyces genes coding for synthesis of different polyketides used to clone antibiotic biosynthetic genes.

Many important antibiotics such as tetracyclines, erythromycin, adriamycin, monensin, rifamycin and avermectins are polyketides. In their biosynthesis, multifunctional synthases catalyse iterated condensation of thio-esters derived from acetate, propionate or butyrate to yield aliphatic chains of varying length and carrying different alkyl substituents. Subsequent modifications, including aromatic or macrolide ring closure or specific methylations or glycosylations, generate further chemical diversity. It has been suggested that, if different polyketide synthases had a common evolutionary origin, cloned DNA coding for one synthase might be used as a hybridization probe for the isolation of others. We show here that this is indeed possible. Study of a range of such synthase genes and their products should help to elucidate what determines the choice and order of condensation of different residues in polyketide assembly, and might yield, by in vitro recombination or mutagenesis, synthase genes capable of producing novel antibiotics. Moreover, because genes for entire antibiotic pathways are usually clustered in Streptomyces, cloned polyketide synthase genes are valuable in giving access to groups of linked biosynthetic genes.

Anthraquinones↗
PubMedDate not supplied

Caring for a Marfan patient with cardiovascular complications.

The Marfan syndrome is a heritable disorder of connective tissue associated with characteristic abnormalities of the skeletal, ocular and cardiovascular systems. Common cardiovascular manifestations of this syndrome are mitral valve prolapse with mitral regurgitation and dilatation of the ascending aorta resulting in aortic insufficiency, dissection, aneurysm and/or rupture. Although the prognosis for a patient with the Marfan syndrome is significantly more favorable than it was ten years ago, the cardiovascular complications continue to greatly reduce life expectancy. This article presents an overview of the Marfan syndrome including: history and epidemiology, clinical manifestations, diagnostic criteria, surgical intervention and follow-up. A case study is outlined which focuses on priority nursing diagnoses and a plan of care.

Adult↗
PubMedDate not supplied

Recommended reading for the FRCA diploma. Fellow of the Royal College of Anaesthetists.

Anaesthetists in training have access to a bewildering array of journals and textbooks from which to acquire information for the FRCA diploma. From the results of a questionnaire sent to 60 senior registrars, we have produced a core selection of journals and textbooks to guide the trainee preparing for all three parts of the diploma.

Anesthesiology↗