Localized, Cold-Induced Inhibition of Translocation in Mycelia and Strands of Serpula lacrimans

Thompson, W., Brownlee, C, Jennings, D. H. and Mortimer, A.M. 1987. Localized, cold-induce inhibition of translocationin mycelia and strands of Serpula lacrimans. —J. exp.Bot. 38: 889–899 The effect has been investigated of localized low temperatureon translocation of ³²P across myceliui of Serpula lacrimansusing two gas-flow detectors capable of recording radioactivitycontinuously. When the temperature of a band of mycelium wasreduced to 0 ? C, radioactivity ceased to accumulai and in factdeclined under the detector (number 2) separated from the sourceof radioactivity by tr cold-treated mycelium. In the myceliumbeneath the other detector (number 1), closest to the sourceradioactivity, the rate of accumulation of radioactivity increased.When the temperature was raised t 20 ?C, radioactivity beganto accumulate in the mycelium under detector 2 and, apart froma sma fluctuation, continued to accumulate at a uniform rate.In the mycelium under detector 1, the accumulation of radioactivitystopped for a short time but then recommenced at a rate similarto thi found at 0 ?C. In other experiments the distributionof radioactivity (¹⁴C) throughout the myceliui was measuredat the end in homogenized samples. In these experiments a bandof mycelium we subjected to 0 ?C or to 20 ?C for the whole experimentalperiod, or only after the mycelium had bee translocating radioactivityalready for 16 h. These experiments showed that the changesin the rate of accumulation of ³²P in living mycelium underthe two gas flow detectors used for in situ measurements werenot due to a reversal of the flow of translocation. The resultsare consistent with an hypothesis that a turgor-driven massflow of solution is the mechanism for translocation in thisfungus and are considered in relation to the results of similarexperiments on phloem translocation in higher plants. Key words: Serpula lacrimans, mycelium, translocation, low-temperature, phloem transport     

Internal Structure and Hydraulic Conductivity of Basidiomycete Translocating Organs

Eamus, D., Thompson, W., Cairney, J. W. G. and Jennings, D.H. 1985. Internal structure and hydraulic conductivity of basidiomycetetranslocating organs.–J. exp. Bot. 36: 1110–1116. The presence in rhizomorphs of Armillaria mellea and cords ofPhallus impudicus of wide diameter hyphae (5–20 {diaeresis}m),which run for considerable distances along these linear organs,has been demonstrated. The longitudinal hydraulic conductivityof these organs has been determined experimentally and similarvalues were obtained when the hydraulic conductivity was calculatedtheoretically on the basis that the vessel hyphae were the solechannel for water movement along these organs. The experimentaldata have been discussed in relation to other data for long-distancetranslocation in basidiomycete linear organs. It is concludedthat the vessel hyphae are the main channels for turgor-driventranslocation. Key words: -Basidiomycete fungi, translocation, hydraulic conductivity     

Biochemical and genetic characterization of three hamster cell mutants resistant to diphtheria toxin

We describe here three different hamster cell mutants which are resistant to diphtheria toxin and which provide models for investigating some of the functions required by the toxin inactivates elongation factor 2 (EF-2). Cell-free extracts from mutants Dtx(r)-3 was codominant. The evidence suggests that the codominant phenotype is the result of a mutation in a gene coding for EF-2. The recessive phenotype might arise by alteration of an enzyme which modifies the structure of EF-2 so that it becomes a substrate for reaction with the toxin. Another mutant, Dtx(r)-2, contained EF-2 that was sensitive to the toxin and this phenotype was recessive. Pseudomonas aeruginosa exotoxin is known to inactivate EF-2 as does diphtheria toxin and we tested the mutants for cross-resistance to pseudomonas exotoxin. Dtx(r)-1 and Dtx(r)-3 were cross-resistant while Dtx(r)-2 was not. It is known that diphtheria toxin does not penetrate to the cytoplasm of mouse cells and that these cell have a naturally occurring phenotype of diphtheria toxin resistance. We fused each of the mutants with mouse 3T3 cells and measured the resistance. We fused each of the mutants with mouse 3T3 cells and measured the resistance of the hybrid cells to diphtheria toxin. Intraspecies hybrids containing the genome of mutants Dtx(r)-1 and Dtx(r)-3 had some resistance while those formed with Dtx(r)-2 were as sensitive as hybrids derived from fusions between wild-type hamster cells and mouse 3T3 cells.     

Alterations in osteoclast morphology following osteoprotegerin administration in the magnesium-deficient mouse

In the present study, we used osteoprotegerin (OPG), which blocks osteoclastogenesis, to correct and thus explain the hypercalcemia that is seen during dietary Mg deficiency in the mouse. Control and Mg-deficient mice received injections for 12 days of either OPG or vehicle only. Serum Ca was similar in Mg-deficient mice treated with OPG and in control mice receiving OPG (9.2±0.3 mg/dl vs. 9.2±0.5). Both groups had significantly higher serum Ca than controls or Mg-deficient animals receiving vehicle alone. Surprisingly, Mg-depleted mice that received OPG in doses that inhibit osteoclastic bone resorption remained hypercalcemic. Because mature osteoclasts still present in the marrow might be hyperactive, we examined osteoclast morphology at the light microscopic and ultrastructural level. Light microscopic examination of trabecular bone showed few osteoclasts in OPG-treated mice. Ultrastructural examination revealed that osteoclasts in OPG-treated mice have decreased contact with the endosteal bone surface and absence of a ruffled border. Because the morphology of the existing pool of mature osteoclasts did not enhance resorption, another mechanism, such as increased intestinal absorption of Ca in Mg-deficient mice, likely contributes to the hypercalcemia observed during Mg deficiency.     

Methylation: a regulator of HIV-1 replication?

Pakistan, the second most populous Muslim nation in the world, has started to finally experience and confront the HIV/AIDS epidemic. The country had been relatively safe from any indigenous HIV cases for around two decades, with most of the infections being attributable to deported HIV positive migrants from the Gulf States. However, the virus finally seems to have found a home-base, as evidenced by the recent HIV outbreaks among the injection drug user community. Extremely high-risk behavior has also been documented among Hijras (sex workers) and long-distance truck drivers. The weak government response coupled with the extremely distressing social demographics of this South-Asian republic also helps to compound the problem. The time is ripe now to prepare in advance, to take the appropriate measures to curtail further spread of the disease. If this opportunity is not utilized right now, little if at all could be done later.