Microbial populations and activity in two soils of Tanzania as influenced by mercury

Summary The influence of mercury on microbial populations and activity of two soils from Tanzania was studied. Aretan (2-methoxyethylmercury chloride) slightly affected the microbial population of the Morogoro (Oxisol) soil, which was 10⁷ c.f.u./g in control soil and 10⁶ c.f.u./g in the presence of 2000 mg Hg/kg soil. Mercuric chloride at >8 mg Hg/kg soil increased the population slightly, with a sharp decrease at >100 mg Hg/kg soil, dropping ultimately to 10³ c.f.u./g at 2000 mg Hg/kg soil. In the Arusha (Andept) soil, the microbial response to the two mercury compounds was the opposite of that for the Morogoro soil. Aretan sharply reduced the nitrogenase activity of aerobically incubated Morogoro soils at Hg levels >24 mg/kg, resulting in very low activity at >50 mg Hg/kg soil. Mercuric chloride increased the activity, which showed a peak at 24 mg Hg/kg soils, followed by a sharp drop at 30 mg Hg/kg and remained low thereafter. In the Arusha soil, the activity was reduced gradually by both Aretan and HgCl₂. The response of the activity under anaerobic incubation in the Morogoro soil was the opposite of that under aerobic incubation, in that it was Aretan which at first increased the activity. In the Arusha soil the activity under anaerobic incubation decreased gradually over the entire range of added Hg. Nitrification was decreased by HgCl₂ atlevels of <2 and <10 mg Hg/kg soil in the Arusha and Morogoro soils, respectively. The tolerance to Hg by microorganisms in this study was in the order: total population > nitrogen fixers > nitrifiers. This may be explained in terms of species diversity of the microorganisms, which may be expected to follow the same sequence.

---

Population et activités microbiennes dans deux sols de Tanzanie sous l'influence du mercure

Résumé On étudie l'influence du mercure sur les populations et les activités microbiennes de deux sols en provenance de Tanzanie. L'Aretan (chlorure de 2-méthoxyéthylmercure) n'affecte que faiblement la population microbienne du sol de Morogoro (oxisol), qui compte 10⁷ individus par g dans le sol témoin et 10⁶ individus en présence de 2000 mg de mercure par kg de sol. Le chlorure mercurique, à une dose supérieure à 8 mg de mercure par kg de sol, augmente quelque peu la population. Celle-ci décroît brutalement au delà de 100 mg de mercure par kg de sol, pour tomber finalement à 10³ individus par g à 2000 mg de mercure par kg de sol. Dans le sol d'Arusha (Andept), la réponse microbienne aux deux composés mercuriels est l'inverse de celle obtenue avec le sol de Morogoro. L'Aretan réduit fortement l'activité de la nitrogénase de sols de Morogoro incubés en aérobiose à des teneurs en mercure au delà de 24 mg par kg. L'activité devient très faible au delà de 50 mg de mercure par kg de sol. Le chlorure mercurique augmente cette activité, avec un pic de 24 mg de mercure par kg de sol, suivi d'une chute sévère à 30 mg de mercure par kg. L'activité demeure faible aux doses plus fortes. Dans le sol d'Arusha, l'activité est réduite progressivement tant par l'Aretan que par HgCl₂. La réponse de l'activité en incubation anaérobie dans le sol de Morogoro est l'inverse de celle en incubation aérobie en ceci que c'est l'Aretan, cette fois-ci, qui augmente d'abord l'activité. Dans le sol d'Arusha, l'activité en incubation anaérobie décroît progressivement sur l'échelle entière des concentrations d'ajout de mercure. La nitrification est réduite par HgCl₂ à des seuils au dessous de 2 et 10 mg de mercure par kg de sol, respectivement pour les sols d'Arusha et de Morogoro. La tolérance des microorganismes au mercure dans cette étude est dans l'ordre: population totale > fixateurs d'azote > nitrificateurs. Ceci peut être expliqué en termes de diversité des espèces de microorganismes qui suit vraisemblablement la même séquence.

     

Further studies of the plasma alpha 1 B-glycoprotein polymorphism: two new alleles and allele frequencies in Caucasians and in American blacks

Two new alleles (A1 B*3 and A1 B*4) of human plasma alpha 1 B-glycoprotein (alpha 1 B) were reported. alpha 1 B phenotyping was done by using either a simple method of two-dimensional (2-D) agarose gel-horizontal polyacrylamide gel electrophoresis (PAGE) followed by protein staining or by one-dimensional horizontal PAGE and immunoblotting. Seven different alpha 1 B phenotypes (1-1, 1-2, 1-3, 1-4, 2-2, 2-3 and 3-3) were observed; phenotypes 1-3 and 1-4 were differentiated from each other only by the 2-D method. The respective frequencies Af A1 B*1, A1 B*2, A1 B*3 and A1 B*4 alleles in the studied populations were estimated as follows: American Blacks (New York) 0.732, 0.204, 0.064, 0; American Whites (New York) 0.947, 0.053; Czechs (M?lník) 0.964, 0.034, 0, 0.002; Slovaks (Bratislava and Trencin) 0.977, 0.023, 0, 0. The population of American Blacks showed a much higher degree of alpha 1 B polymorphism (polymorphism information content = 0.37) than the Caucasian populations that have been studied.     

Analysis of HLA and Disease Susceptibility: Chromosome 6 Genes and Sex Influence Long-QT Phenotype

The long-QT (LQT) syndrome is a genetically complex disorder that is characterized by syncope and fatal ventricular arrhythmias. LQT syndrome, as defined by a prolonged electrocardiographic QT interval, has a higher incidence in females than in males and does not exhibit Mendelian transmission patterns in all families. Among those families that are nearly consistent with Mendelian transmission, linkage between a locus for LQT syndrome and the H-ras-1 locus on the short arm of chromosome 11 has been reported in some families but not in others. Earlier analyses suggesting that LQT syndrome might be caused by a gene in the HLA region of chromosome 6 were not confirmed by standard linkage analyses. Here, we present an analysis of HLA haplotype sharing among affected pedigree members, showing an excess of haplotype sharing in a previously published Japanese pedigree and possibly also in 15 families of European descent. The haplotypes shared by affected individuals derive from both affected and unaffected parents. In an analysis of independent (unrelated) HLA haplotypes, we also found a nonrandom distribution of HLA-DR genes in LQT syndrome patients compared with controls, suggesting an association between the LQT phenotype and specific HLA-DR genes. Our data indicate that DR2 has a protective effect and, particularly in males, that DR7 may increase susceptibility to the LQT syndrome. Thus, LQT syndrome may be influenced by genes on chromosomes 11 and 6, possibly with a sex-specific effect. These results provide a model for an effect of HLA-region genes inherited from either parent on the expression of an illness that may be determined principally by alleles at loci not linked to HLA.     

Silencing of EEF2K (eukaryotic elongation factor-2 kinase) reveals AMPK-ULK1-dependent autophagy in colon cancer cells

EEF2K (eukaryotic elongation factor-2 kinase), also known as Ca²⁺/calmodulin-dependent protein kinase III, functions in downregulating peptide chain elongation through inactivation of EEF2 (eukaryotic translation elongation factor 2). Currently, there is a limited amount of information on the promotion of autophagic survival by EEF2K in breast and glioblastoma cell lines. However, the precise role of EEF2K in carcinogenesis as well as the underlying mechanism involved is still poorly understood. In this study, contrary to the reported autophagy-promoting activity of EEF2K in certain cancer cells, EEF2K is shown to negatively regulate autophagy in human colon cancer cells as indicated by the increase of LC3-II levels, the accumulation of LC3 dots per cell, and the promotion of autophagic flux in EEF2K knockdown cells. EEF2K negatively regulates cell viability, clonogenicity, cell proliferation, and cell size in colon cancer cells. Autophagy induced by EEF2K silencing promotes cell survival and does not potentiate the anticancer efficacy of the AKT inhibitor MK-2206. In addition, autophagy induced by silencing of EEF2K is attributed to induction of protein synthesis and activation of the AMPK-ULK1 pathway, independent of the suppression of MTOR activity and ROS generation. Knockdown of AMPK or ULK1 significantly abrogates EEF2K silencing-induced increase of LC3-II levels, accumulation of LC3 dots per cell as well as cell proliferation in colon cancer cells. In conclusion, silencing of EEF2K promotes autophagic survival via activation of the AMPK-ULK1 pathway in colon cancer cells. This finding suggests that upregulation of EEF2K activity may constitute a novel approach for the treatment of human colon cancer.     

Impaired antibody response to group B streptococcal type III capsular polysaccharide in C3- and complement receptor 2-deficient mice

Group B Streptococcus (GBS) is the foremost bacterial cause of serious neonatal infections. Protective immunity to GBS is mediated by specific Abs to the organism's capsular polysaccharide Ags. To examine the role of complement in the humoral immune response to type III GBS capsular polysaccharide (III-PS), mice deficient in C3 or in CD21/CD35 (i.e., complement receptors 1 and 2; CR1/CR2) were immunized with III-PS. Mice deficient in C3 or Cr2 had an impaired primary immune response to III-PS. The defective response was characterized by low IgM levels and the lack of an isotype switch from IgM to IgG Ab production. Compared with wild-type mice, C3- and Cr2-deficient mice exhibited decreased uptake of III-PS by follicular dendritic cells within the germinal centers and impaired localization of III-PS to the marginal zone B cells. Complement-dependent uptake of capsular polysaccharide by marginal zone B cells appears necessary for an effective immune response to III-PS. The normal immune response in wild-type mice may require localization of polysaccharide to marginal zone B cells with subsequent transfer of the Ag to follicular dendritic cells.