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At least 73 records · Page 4Linked to original sources
PubMed2003

Expressed sequence tag (EST) analysis of two subspecies of Metarhizium anisopliae reveals a plethora of secreted proteins with potential activity in insect hosts.

Expressed sequence tag (EST) libraries for Metarhizium anisopliae, the causative agent of green muscardine disease, were developed from the broad host-range pathogen Metarhizium anisopliae sf. anisopliae and the specific grasshopper pathogen, M. anisopliae sf. acridum. Approximately 1,700 5' end sequences from each subspecies were generated from cDNA libraries representing fungi grown under conditions that maximize secretion of cuticle-degrading enzymes. Both subspecies had ESTs for virtually all pathogenicity-related genes cloned to date from M. anisopliae, but many novel genes encoding potential virulence factors were also tagged. Enzymes with potential targets in the insect host included proteases, chitinases, phospholipases, lipases, esterases, phosphatases and enzymes producing toxic secondary metabolites. A diverse array of proteases composed 36 % of all M. anisopliae sf. anisopliae ESTs. Eighty percent of the ESTs that could be clustered into functional groups had significant matches (E<10(-5)) in other ascomycete fungi. These included genes reported to have specific roles in pathogens with plant or vertebrate hosts. Many of the remaining ESTs had their best BLAST match among animal, plant and bacterial sequences. These include genes with plant and microbial counterparts that produce potent antimicrobials. The abundance of transcripts discovered for different functional groups varied between the two subspecies of M. anisopliae in a manner consistent with ecological adaptations of the two pathogens. By hastening gene discovery this project has enhanced development of improved mycoinsecticides. In addition, the M. anisopliae ESTs represent a significant contribution to the extensive database of sequences from ascomycetes that are saprophytes or plant and vertebrate pathogens. Comparative analyses of these sequences is providing important information about the biology and evolutionary history of this clade.

Animals↗
PubMed2003

Mitochondrial differentiation in kinetoplastid protozoa: a plethora of RNA controls.

Differentiation of kinetoplastid protozoa during their complex life cycles is accompanied by stepwise changes in mitochondrial functions. Recent studies have begun to reveal multilevel post-transcriptional regulatory mechanisms by which the expression of the nuclear and mitochondrially encoded components of respiratory enzymes is coordinated, as well as the identities of some general and gene-specific factors controlling mitochondrial differentiation.

Animals↗
PubMed1995

A plethora of cardiac chloride conductances: molecular diversity or a related gene family.

Recent electrophysiologic studies have provided evidence suggesting that as many as six different Cl- conductances can be identified in the sarcolemma of cardiac myocytes isolated from various animal species and areas of the heart. These include Cl- conductances activated by stimulation of protein kinase A, protein kinase C, extracellular ATP, intracellular Ca2+, membrane stretch, and a basally active Cl- conductance. Many basic biophysical and pharmacological properties of these channels are presently unknown, and the only molecular information presently available suggests that the cAMP-activated Cl- conductance is due to cardiac expression of an isoform of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel normally found in epithelial cells. We used the polymerase chain reaction (PCR) to amplify four distinct regions corresponding to the cardiac CFTR gene product from several cardiac tissues to determine if the molecular distribution of CFTR matches the distribution of cAMP-dependent Cl- channels in native myocytes. Amplification of regions corresponding to the first nucleotide binding domain (NBD1), transmembrane segments (TS) VII-XII, and the regulatory (R) domain showed a precise correlation to tissues that electrophysiologically exhibit sarcolemmal cAMP-dependent Cl- channels, whereas region TS I-VI exhibited a distribution independent of the presence of cAMP-dependent Cl- channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Maintenance and integrity of the mitochondrial genome: a plethora of nuclear genes in the budding yeast.

Instability of the mitochondrial genome (mtDNA) is a general problem from yeasts to humans. However, its genetic control is not well documented except in the yeast Saccharomyces cerevisiae. From the discovery, 50 years ago, of the petite mutants by Ephrussi and his coworkers, it has been shown that more than 100 nuclear genes directly or indirectly influence the fate of the rho(+) mtDNA. It is not surprising that mutations in genes involved in mtDNA metabolism (replication, repair, and recombination) can cause a complete loss of mtDNA (rho(0) petites) and/or lead to truncated forms (rho(-)) of this genome. However, most loss-of-function mutations which increase yeast mtDNA instability act indirectly: they lie in genes controlling functions as diverse as mitochondrial translation, ATP synthase, iron homeostasis, fatty acid metabolism, mitochondrial morphology, and so on. In a few cases it has been shown that gene overexpression increases the levels of petite mutants. Mutations in other genes are lethal in the absence of a functional mtDNA and thus convert this petite-positive yeast into a petite-negative form: petite cells cannot be recovered in these genetic contexts. Most of the data are explained if one assumes that the maintenance of the rho(+) genome depends on a centromere-like structure dispensable for the maintenance of rho(-) mtDNA and/or the function of mitochondrially encoded ATP synthase subunits, especially ATP6. In fact, the real challenge for the next 50 years will be to assemble the pieces of this puzzle by using yeast and to use complementary models, especially in strict aerobes.

Adenosine Triphosphatases↗
PubMed1977

Radiological findings in symptomatic neonatal plethora resulting from placental transfusion.

As a result of excessive placental transfusion at birth, 8 premature and 3 full-term infants presented with cardiorespiratory and neurological symptoms. Cord clamping was delayed in all infants, and blood volume studies showed polycythemia or hypervolemia. The radiological findings included pulmonary vascular congestion, hyperaeration, pleural effusion, and mild cardiomegaly. Most infants responded to conservative medical management and were asymptomatic within 24 to 72 hours. Three acutely ill infants showed great improvement after phlebotomy, providing further evidence that circulatory overload due to placental transfusion may be the etiological factor in this symptom-complex.

Heart Failure↗
PubMed1993

A plethora of GTPases, large and small.

It has become apparent recently that a variety of small GTPases (small GTP-binding proteins or smgs), related to the oncogene ras, are involved in many cellular functions, especially membrane traffic and cytoskeleton regulation. This review will summarize some of the major themes that are emerging, focusing on the presence and possible functions of these smgs in the gastrointestinal tract. In addition, new cellular locations and functions for heterotrimeric G-proteins, previously believed to be solely associated with plasma membrane receptors, are becoming evident and will be discussed here.

Animals↗
PubMed1990

Current and future drugs for acid-peptic disease: a plethora of opinions on possible mechanisms of action.

Sixty-seven invited participants involved in the development, evaluation, and use of therapies for acid-peptic disorders participated in a meeting to discuss the scientific basis for healing actions of ulcer drugs and the prospects for future developments ("Realities of Mucosal Protection in the Upper Gastrointestinal Tract," Lausanne, Switzerland, November 8-10, 1987). Eighty-one key statements were prepared and subsequently analyzed on the basis of a voting system. Of the 45 statements that dealt with existing therapies, only 3 statements showed positive consensus (agreement of two-thirds or more of voters) about mechanisms of ulcer healing. Participants agreed that both (1) hydrogen/potassium adenosine triphosphatase inhibitors and (2) histamine H2 antagonists healed ulcers solely by acid inhibition, and (3) that sucralfate works by topical action. Substantial uncertainty about the mechanisms by which bismuth compounds and antacids heal ulcers was noted as well as their wide range of effects. The mechanism of ulcer healing by prostaglandins and the clinical relevance of antiulcer effects of drugs demonstrated in acute studies with animals were also controversial. There was greater agreement among participants about unexplored drug effects that might produce ulcer healing. Of the 36 such mechanisms surveyed, the most support went to therapies aimed at enhancement of mucosal blood flow, epithelial restitution, and mucosal alkaline secretion or inhibition of luminal pepsin activity. The diversity of opinions among participants suggests a high level of empiricism in the development of ulcer healing drugs apart from those that inhibit acid secretion. This empiricism probably arises from inadequate understanding of processes of mucosal injury and repair.

Drug Design↗