Biotransformation of squamulosone by Curvularia lunata ATCC 12017

Squamulosone (aromadendr-1(10)-en-9-one), isolated in large quantity from the plant Hyptis verticillata Jacq. (Labiatae), was incubated with the fungus Curvularia lunata ATCC 12017 in two different growth media. Six metabolites were isolated from each medium. with five of the products being common to both fermentations. All seven metabolites are novel. The insecticidal activity of these aromadendranes was evaluated against the sweet potato weevil Cylas formicarius elegantus.     

Biotransformation of cedrol by Curvularia lunata ATCC 12017

Bioconversion of cedrol (1) with the Curvularia lunata was investigated in two different growth media. Five products were obtained in potato dextrose broth, whereas nine compounds were produced in a medium containing beef extract. Only three of the metabolites: 3beta-hydroxycedrol (2), 3alpha-hydroxycedrol (3) and 12-hydroxycedrol (4) were common to both media. They were also obtained as the major products in each case. Three new derivatives have also been identified.     

Steroid transformations with Fusarium oxysporum var. cubense and Colletotrichum musae

The utility of two locally isolated fungi, pathogenic to banana, for steroid biotransformation has been studied. The deuteromycetes Fusarium oxysporum var. cubense (IMI 326069, UAMH 9013) and Colletotrichum musae (IMI 374528, UAMH 8929) had not been examined previously for this potential. In general, F. oxysporum var. cubense effected 7alpha hydroxylation on 3beta-hydroxy-delta5-steroids, 6beta, 12beta, and 15alpha hydroxylation on steroidal-4-ene-3-ones, side-chain degradation on 17alpha,21-dihydroxypregnene-3,20-diones, and 15alpha hydroxylation on estrone. Both strains were shown to perform redox reactions on alcohols and ketones.     

Patency of the preterm fetal ductus arteriosus is regulated by endothelial nitric oxide synthase and is independent of vasa vasorum in the mouse

Patency of the fetal ductus arteriosus (DA) is maintained in an environment of low relative oxygen tension and a preponderance of vasodilating forces. In addition to prostaglandins, nitric oxide (NO), a potent vasodilator in the pulmonary and systemic vasculatures, has been implicated in regulation of the fetal DA. To further define the contribution of NO to DA patency, the expression and function of NO synthase (NOS) isoforms were examined in the mouse DA on days 17-19 of pregnancy and after birth. Our results show that endothelial NOS (eNOS) is the predominant isoform expressed in the mouse DA and is localized in the DA endothelium by in situ hybridization. Despite rapid constriction of the DA after birth, eNOS expression levels were unchanged throughout the fetal and postnatal period. Pharmacological inhibition of prostaglandin vs. NO synthesis in vivo showed that the preterm fetal DA on day 16 is more sensitive to NOS inhibition than the mature fetal DA on day 19, whereas prostaglandin inhibition results in marked DA constriction on day 19 but minimal effects on the day 16 DA. Combined prostaglandin and NO inhibition caused additional DA constriction on day 16. The contribution of vasa vasorum to DA regulation was also examined. Immunoreactive platelet endothelial cell adhesion molecule and lacZ tagged FLK1 localized to DA endothelial cells but revealed the absence of vasa vasorum within the DA wall. Similarly, there was no evidence of vasa vasorum by vascular casting. These studies indicate that eNOS is the primary source of NO in the mouse DA and that vasomotor tone of the preterm fetal mouse DA is regulated by eNOS-derived NO and is potentiated by prostaglandins. In contrast to other species, mechanisms for DA patency and closure appear to be independent of any contribution of the vasa vasorum.     

Investigation of the importance of the C-2 oxygen function in the transformation of stemodin analogues by Rhizopus oryzae ATCC 11145

A new stemodinoside, stemodin-alpha-L-arabinofuranoside (5), was isolated from the plant Stemodia maritima. Incubation of stemodin (2) with Rhizopus oryzae ATCC 11145 gave 2 alpha,7 beta,13(S)-trihydroxystemodane (17) and 2 alpha,3 beta,13(S),16 alpha-tetrahydroxystemodane (18) whilst stemodinone (8) afforded 6 alpha,13(S)-dihydroxystemodan-2-one (19). The bioconversion of 2 beta,13(S)-dihydroxystemodane (10) by the fungus yielded 2 beta,7 beta,13(S)-trihydroxystemodane (20) whereas stemod-12-en-2-one (9) provided 7 beta,17-dihydroxystemod-12-en-2-one (21). The results provide useful information about the relationship between the functional groups of the substrates and their potential for bioconversion.     

Bves: prototype of a new class of cell adhesion molecules expressed during coronary artery development

Bves is a protein expressed in cells of the developing coronary vascular system, specifically in the proepicardium, migrating epithelial epicardium, delaminated vasculogenic mesenchyme and vascular smooth muscle cells. Here, we show that Bves protein undergoes a dynamic subcellular redistribution during coronary vessel development. Bves is a membrane protein with three predicted transmembrane helices, an extracellular C terminus and an intracellular N terminus, and is confined to the lateral membrane compartment of epithelial cells. When epicardial cells are dissociated into single cells in vitro, Bves accumulates in a perinuclear region until cells make contact, at which time Bves is trafficked to the cell membrane. Bves accumulates at points of cell/cell contact, such as filopodia and cell borders, before the appearance of E-cadherin, suggesting an early role in cell adhesion. While Bves shares no homology with any known adhesion molecule, transfection of Bves into L-cells readily confers adhesive behavior to these cells. Finally, Bves antibodies inhibit epithelial migration of vasculogenic cells from the proepicardium. This study provides direct evidence that Bves is a novel cell adhesion molecule and suggests a role for Bves in coronary vasculogenesis.     

Escalation and extinction selectivity: morphology versus isotopic reconstruction of bivalve metabolism

Studies that have tested and failed to support the hypothesis that escalated species (e.g., those with predation-resistant adaptations) are more susceptible to elimination during mass extinctions have concentrated on the distribution and degree of morphological defenses in molluscan species. This morphological approach to determining level of escalation in bivalves may be oversimplified because it does not account for metabolic rate, which is an important measure of escalation that is less readily accessible for fossils. Shell growth rates in living bivalves are positively correlated with metabolic rate and thus are potential indicators of level of escalation. To evaluate this approach, we used oxygen isotopes to reconstruct shell growth rates for two bivalve species (Macrocallista marylandica and Glossus markoei) from Miocene-aged sediments of Maryland. Although both species are classified as non-escalated based on morphology, the isotopic data indicate that M. marylandica was a faster-growing species with a higher metabolic rate and G. markoei was a slower-growing species with a lower metabolic rate. Based on these results, we predict that some morphologically non-escalated species in previous tests of extinction selectivity should be reclassified as escalated because of their fast shell growth rates (i.e., high metabolic rates). Studies that evaluate the level of escalation of a fauna should take into account the energetic physiology of taxa to avoid misleading results.