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In a previous study on the chemostat culture of Saccharomyces carlsbergensis, maximum invertase specific activity was observed at an intermediate dilution rate. A possible regulation mechanism, assuming there are simultaneous effects of induction and repression on two sites of the operator loci for invertase formation, is proposed which might account for the observed curve of the dilution rate effect.
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Natural and induced cell degeneration were studied in the mesencephalic parabigeminal nucleus of postnatally developing rats. Natural cell death in the normal parabigeminal nucleus had already started at birth, was maximal at 3 days, and proceeded with a declining rate until postnatal days 8-10 in the dorsal, middle, and ventral divisions that compose the nucleus. The number of neurons declined by approximately one-third between birth and postnatal day 15. A unilateral lesion of the superior colliculus made at birth modified this pattern. In the deafferented ipsilateral middle division, the rate of cell death was above normal from day 1 to day 10, and the number of neurons at day 15 was 60% less than in unoperated controls. In the contralateral middle division, in which at least some of the neurons were axotomized by the lesion, the rate of cell death increased at days 1-2 and decreased below normal at days 3-5. Induced changes in the number of neurons were consistent with this pattern, and at day 15 the number was similar to the control value. In the ipsilateral dorsal and ventral divisions, which suffered simultaneous axotomy and deafferentation, the rate of cell death increased in 2 peaks at days 1-2 and 4-6, and the numbers of neurons dropped to negligible values at day 15. The frequency curves of degenerating cells were poor predictors of the absolute changes in neuron numbers, and evidence was found of continued postnatal migration of neurons into the developing parabigeminal nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)
Human C-reactive protein (CRP) is the major acute phase reactant during acute inflammation. The human CRP promoter is expressed in an inducible and cell-specific manner when linked to the bacterial CAT gene and transfected into human hepatoma cell cultures. In this paper we analyze the effect of several recombinant cytokines or CRP promoter inducibility in human Hep3B cells. When cytokines are tested singly the major inducer of CRP-CAT fusions is interleukin-6 (IL-6). Maximal CAT gene expression, however, is only achieved when both interleukin-1 beta (IL-1 beta) and IL-6 are present. The response to the two cytokines is cooperative. Cooperativity is maintained when the CRP promoter is linked to a different coding region, that of the bacterial neomycin phosphotransferase II gene. With a series of 5' and 3' deletions we show the existence of two distinct and independent regions responsive to IL-6 and located upstream to the TATA box. The IL-1 effect is exerted at the level of downstream sequences that are probably important for optimal mRNA translatability or nuclear-cytoplasmic transport. Inducibility is not influenced by the activation of protein kinases C or A and does not require new protein synthesis.
The trimeric G(i3) protein-dependent lysosomal-autophagic pathway is responsible for the degradation of a pool of N-linked glycoproteins in the human colon cancer HT-29 cell line. Here we have followed the fate of N-glycans using HT-29 cells either overexpressing the wild-type G alpha(i3) protein or transfected with different mutants of the G alpha(i3) protein. The stabilization of N-glycans was dependent upon the inhibition of autophagic sequestration by either 3-methyladenine (3-MA) or pertussis toxin (PTX). However, PTX allowed the processing of high-mannose glycans whereas 3-MA did not. The destabilization of the Golgi apparatus by brefeldin A, which interrupts the intracellular trafficking of N-linked glycoproteins along the secretory pathway, did not interfere with the macroautophagic pathway. These results suggest that the lysosomal-autophagic pathway is not dependent upon the integrity of the Golgi apparatus and points to differences between the molecular properties of two membrane flow processes (macroautophagy, exocytic pathway) controlled by the trimeric G(i3) protein.
Two inositol phosphoglycans (IPG) isolated from beef liver and designated as putative insulin mediators were demonstrated to reciprocally enhance the dephosphorylation of inhibitor-1 (INH-1) and DARPP-32, thus directly activating phosphatase 2C and disinhibiting phosphatase 1 in a potential protein phosphatase 2C --> phosphatase 1 cascade mechanism. One IPG termed pH 2.0, containing Dchiro-inositol and galactosamine, stimulated the dephosphorylation of INH-1 and DARPP-32 in a dose-dependent manner in the low micromolar range. A second, termed pH 1.3, containing myo-inositol glucosamine and mannose acted reciprocally to inhibit the cAMP-dependent protein kinase phosphorylation of INH-1 and DARPP-32 in a dose-dependent manner in the low micromolar range. These model experiments are discussed in terms of the observed dephosphorylation of INH-1 with insulin action documented in the literature and the activation of both phosphatase 1 and 2C described in intact cells and in vivo with insulin action.
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The timing of host-cell lysis by coliphage lambda is controlled by two separable systems. The lambdaS gene product acts as a positive effector of lysis while another protein, the lysis regulator, is an inhibitor of lysis. If the continuous function of the lysis regulator is interrupted in phage infected cells immediate lysis ensues. This lysis requires metabolic energy but not S gene activity. In contrast, S protein activity is stimulated by agents which uncouple and which block oxidative phosphorylation. The lysis regulator is thermolabile and several lines of evidence suggest that it may be the lambdarex gene product.
Gonadotropic hormones PMSG (15 IU/rat), FSH (3 micrograms/rat), LH (9 micrograms/rat) and hCG (3 micrograms/rat) were shown to decrease the free cytosolic lysosomal enzymes during the acute phase of hormone action in rat ovaries. When isolated cells from such rats were analyzed for the cathepsin-D activity, the granulosa cells of the ovary showed a reduction in the free as well as in the total lysosomal enzyme activities in response to FSH/PMSG; the stromal and thecal compartment of the ovary showed a reduction only in the free activity in response to hCG/PMSG. The results suggest the presence of two distinct, target cell specific, mechanisms by which the lysosomal activity of the ovary is regulated by gonadotropins.
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Whole-cell and single-channel recordings were used to study an ionic current activated by extracellular adenosine 5'-triphosphate (ATP) applied to calf atrial cells. ATP (Kd approximately 10 microM) elicited an inwardly rectifying current that reversed near EK and was blocked by external Cs+ (10 mM). Under identical conditions, adenosine had no effect. Cell-attached patch recordings revealed an ATP-activated channel with a slope conductance of about 30 pS. At both the whole-cell and single-channel levels, the channels activated by ATP seemed nearly identical to the potassium channels activated by acetylcholine (ACh) in the same cells. However, the effects of ATP were not affected by atropine, suggesting that ATP does not interact with the same receptors as ACh. In some cells, whole-cell currents of similar magnitude were activated by ACh alone, ATP alone, or ACh and ATP applied together. These results suggest that calf atrial cells possess a population of inwardly rectifying potassium channels that are controlled jointly by two populations of receptors selective for ACh and ATP.
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The gene katX, which encodes a catalase in Bacillus subtilis, is transcribed by EsigmaF in the pre-spore. This catalase is responsible for the resistance to hydrogen peroxide shown by germinating and outgrowing spores. We demonstrated that katX is also a sigmaB-dependent general stress gene, since it is strongly induced by heat, salt and ethanol stress, as well as by energy depletion. The -10 and -35 sequences of the sigmaB- and sigmaF-dependent promoters of katX overlap, and the transcriptional start points used by EsigmaB and EsigmaF differ by only one nucleotide. Our results indicate that the level of KatX level in outgrowing spores depends mainly on EsigmaF, because sigB mutants show normal KatX activity in dormant and outgrowing spores. katX mutants also develop the non-specific resistance to oxidative stress that is typical of glucose-starved cells. Therefore, the physiological role of sigmaB-dependent katX expression remains obscure. The results indicate an overlap between the sigmaB regulon and the sigmaF regulon, and the physiological implications of this overlap are discussed.
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Fructose 2,6-bisphosphate, the most potent activator of 6-phosphofructo-1-kinase, has been demonstrated to mediate the increase of glycolytic flux induced by mitogens human fibroblasts. In the present work the molecular basis of transmembrane control of fructose 2,6-bisphosphate has been investigated. Prostacyclin and isoprenaline, known to activate adenylate cyclase, are able to increase fructose 2,6-bisphosphate levels, indicating that in human fibroblasts cyclic AMP plays a positive role in the control of the metabolite concentration, opposite to that exerted in hepatocytes. Substances known to activate protein kinase C such as phorbol 12-myristate 13-acetate, or to stimulate phosphoinositide turnover such as thrombin and bradykinin are also effective in raising fructose 2,6-bisphosphate. Therefore, we conclude that cyclic AMP and protein kinase C are likely involved in the control of fructose 2,6-bisphosphate levels in human fibroblasts.
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Explore the source record for details and available documents.