Publications by authors named "BRODY S"

Nuclear mutations conferring resistance to oligomycin, a mitochondrial inhibitor, shorten the period of the circadian conidiation rhythm of Neurospora crassa from the normal 21.5 hours to 18 to 19 hours and slow the linear growth rate by 30 percent. These olir mutations map very close to frq, a locus at which mutations affecting periodicity have been previously obtained.

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To assess their effects on the conidiation rhythm in Neurospora, 14 saturated fatty acids from 6 to 24 carbons long were used to supplement the bd csp and bd csp cel strains. Both strains express a circadian spore-forming rhythm when grown on solid media; the cel mutation confers a partial fatty acid requirement. Fatty acid supplements from 8 to 13 carbons long lengthened the free-running period of bd csp cel compared with the control value of 21 h; the maximal effect (33 h) was obtained with nonanoic acid (9:0) at a concentration of 5 x 10(-4) M.

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An inositol deficiency in the inositol-requiring (inl) mutant of Neurospora crassa led to changes in the composition of the inositol-containing lipids and the cell wall. On deficient levels of inositol, phosphatidyl inositol decreased by 23-fold, di(inositolphosphoryl) ceramide decreased by 4-fold, and monoinositolphosphoryl ceramide increased slightly. The inositol deficiency also led to an aberrant hyphal morphology and changes in both the amount of cell wall and the amino sugar content of the cell wall.

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Employing a fatty acid-requiring strain (bd csp cel) of Neurospora crassa, the 21.5-h period of the circadian spore-forming rhythm was manipulated by fatty acid supplementation. The addition to the medium of an unsaturated fatty acid (oleic, linoleic, or linolenic acid) lengthened the period to 26, 40, or 33 h, respectively.

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Ungerminated Neurospora crassa conidia were incubated at 0, 50, and 100% relative humidity, giving rise to conidia in dry, quasi-dry, and wet hydration states, respectively. Metabolic activity was detected by monitoring levels of reduced glutathione (GSH), oxidized glutathione (GSSG), and the soluble-amino acid pools as a function of incubation time. Wet conidia (approximately 65% water content) exhibited significant metabolic activity as evidenced by: (i) reduction of GSSG to GSH, (ii) degradation of GSH, and (iii) changes in the pool sizes of certain amino acids.

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Chlorophyll a monolayers are studied at a nitrogen-water interface in the presence of a reducing or oxidizing agent: sodium ascorbate and benzyl viologen, respectively. Absorption spectra of the films are measured directly on the aqueous surface. With the aid of a computer, fourth derivative and difference spectra are determined.

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Radionuclide techniques for sizing acute myocardial infarction have been hampered by the intrinsic limitations of the scintillation camera. Emission computed tomography can overcome these limitations. Single photon emission computed tomograms of the distribution of technetium-99m pyrophosphate in acute anterior and posterior infarcts were obtained in 16 dogs after death.

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Single-photon emission computed tomography (ECT) was evaluated during myocardial studies in dogs. Acute anterior and posterior infarcts were imaged following injection of 99mTc-pyrophosphate or 201Tl. In most cases, tomographic delineation of infarct location and extent correlated with tissue section.

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Surface properties of monomolecular films of chlorophyll (Chl), plastocyanin (Pc), cytochrome c (Cyt) and ferridoxin (Fd) were measured at a heptane-water interface. Mixed films of Chl and the other components were examined in darkness and in light. The area/molecule, A, for Fd (from Cl.

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In Neurospora, galactosamine can be released from the cell wall and from an alcohol-soluble compound by acid hydrolysis. All of the detectable alcohol-soluble galactosamine was present as uridine diphospho-2-acetamido-2-deoxy-D-galactose (UDPGalNAc). The results of pulse-labeling studies and enzymatic assays indicated that UDPGalNAc was synthesized via the epimerization of uridine diphospho-2-acetamido-2-de+xy-D-glucose (UDPGlcNAc).

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