Nonadditive interactive effects of polychlorinated biphenyl congeners in rats: role of the 2,3,7,8-tetrachlorodibenzo-p-dioxin receptor

Administration of 3,3',4,4',5,5'-hexa-,3,3',4,4',5-penta-, and 2,3,3'4,4'5-hexa-chlorobiphenyl to immature male Wistar rats caused a thymic atrophy at high dose levels (1.25, 1.0, and 100 mumol/kg, respectively) and induced the hepatic cytochrome P-448 dependent monooxygenases (benzo[a]pyrene hydroxylase and ethoxyresorufin O-deethylase) at both high and low (0.25, 0.01, and 5 mumol/kg, respectively) doses. In contrast, 2,2',4,4',5,5'-hexachlorobiphenyl (HCBP) (300 mumol/kg) did not elicit any of these effects but elevated hepatic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) cytosolic receptor protein levels (threefold) as previously reported. The effects of hepatic receptor modulation by 2,2',4,4',5,5'-HCBP (300 mumol/kg) on the enzyme induction activities of 3,3'4,4',5-penta-, 3,3'4,4',5,5'-hexa-, and 2,3,3',4,4',5-hexa-chlorobiphenyl were dose-dependent; no interactive effects were observed at high (toxic) doses of these compounds, whereas apparent synergistically increased hepatic microsomal monooxygenase induction activities were noted at the lower submaximal induction doses. It was concluded that the increased responsiveness of the rats was due to elevated hepatic 2,3,7,8-TCDD receptor levels.     

A note on the use of microwaves in an improved non-radioactive DNA hybridization procedure for the detection of bacteria in foodstuffs

Foodstuffs were artificially contaminated with Escherichia coli carrying plasmid pBR322, dot blotted onto nylon membranes and briefly subjected to microwaves in the presence of 1·5 mol/l NaC1/0·5 mol/l NaOH. Subsequent hybridization with a biotin-labelled probe specific for pBR322 enabled the detection of cell concentrations > 10⁴ cells/dot blot, equivalent to 2 × 10⁷ cells/g food tested. This shortened and simplified method was effective for all ten foods tested, generated low background levels and should be applicable to a wide range of bacteria.     

Plasmid transfer and behaviour in Acinetobacter calcoaceticus EBF65/65

At least one plasmid from each of the incompatibility groups B, C, FIV, H2/S, I alpha, I delta, P, W and X was shown to be capable of transfer from Escherichia coli K12 to Acinetobacter calcoaceticus EBF65/65. Transfer was influenced by the presence of pAV2 (thought to encode a restriction-modification system) in the recipient strain; however, not all plasmids belonging to a particular incompatibility group behaved identically. All plasmids were unstable to varying degrees in A. calcoaceticus EBF65/65, but under suitable conditions were capable of transfer to further strains of EBF65/65 and re-transfer to E. coli K12. Of 40 recently isolated trimethoprim R plasmids 31 transferred successfully from E. coli K12 to A. calcoaceticus EBF65/65, but 17 of these 31 required the introduction of a second mobilizing plasmid for re-transfer to occur.     

Replication-competent picornaviruses with complete genomic RNA 3' noncoding region deletions.

The genomic RNA 3' noncoding region is believed to be a major cis-acting molecular genetic determinant for regulating picornavirus negative-strand RNA synthesis by promoting replication complex recognition. We report the replication of two picornavirus RNAs harboring complete deletions of the genomic RNA 3' noncoding regions. Our results suggest that while specific 3'-terminal RNA sequences and/or secondary structures may have evolved to promote or regulate negative-strand RNA synthesis, the basic mechanism of replication initiation is not strictly template specific and may rely primarily upon the proximity of newly translated viral replication proteins to the 3' terminus of template RNAs within tight membranous replication complexes.     

Duplication of the segment q12.2→qter of chromosome 22 due to paternal inversion 22(p13q12.2)

Summary A 1730-g male infant, born at 37 weeks gestation, had multiple congenital anomalies, consisting of microcephaly, hypertelorism, bilateral cleft lip and palate, micrognathia, lowset ears, and cryptorchidism. Chromosome analysis showed a recombinant 22 derived from the paternal inversion (22) (p13q12.2). The proband's karyotype is 46,XY,rec(22),dup q,inv(22)(p13q12.2)pat, which has a duplication of q12.2qter. An identical recombinant has been reported in a female infant in Mexico whose mother was a carrier of the inversion. Similar congenital anomalies present in these two patients demonstrate the phenotype of duplication of the distal long arm 22. This report also documents the occurrence of an identical inversion in two apparently unrelated Mexican families.     

Tn916 insertion mutagenesis in Escherichia coli and Haemophilus influenzae type b following conjugative transfer.

Transposon Tn916 was shown to be capable of direct conjugative transfer in broth and membrane matings between strains of Escherichia coli K12 and between E. coli K12 and Haemophilus influenzae type b. Only Tn916 was transferred, but Tn916 donor ability was not itself inheritable by the recipients and seemed to be associated with the presence of Tn916 on a non-conjugative pBR322-derived vector in the original donor strain. Transfer of Tn916 by conjugation was found to be an efficient method for producing insertion mutations in the chromosome of recipient cells. Although such insertions were unstable when the cells were grown under non-selective conditions, it was possible to show that over 40% of the isolated Tn916 insertions in the chromosome of E. coli K12 were in gene(s) concerned with histidine biosynthesis, implying that there is a partial hot-spot for Tn916 insertion on the E. coli K12 chromosome. When a strain of H. influenzae type b was used as a recipient, out of approximately 1500 transconjugants tested, two mutants were isolated with insertions in genes controlling the expression of iron-regulated transferrin-binding proteins. These mutants constitutively produced major 76 kDa and minor 90 kDa proteins which bound transferrin, even when grown under iron-sufficient conditions. Tn916 insertion mutagenesis, following transfer by conjugation, is a convenient method for isolating mutations in genes concerned with iron acquisition by this important human pathogen.     

CYTOGENETICS OF TAGETES JALISCENSIS x T. ERECTA

Towner , Joseph W. (U. California, Los Angeles.) Cytogenetics of Tagetes jaliscensis X T. erecta. Amer. Jour. Bot. 49(10): 1064–1067. Illus. 1962.—Although Tagetes jaliscensis and T. erecta are morphologically very distinct, the F₁ hybrid between them had normal meiosis (12 bivalents) and was fertile. Segregation in F₂ was undisturbed for marker genes on 4 pairs of chromosomes. These facts suggest that T. jaliscensis, like T. erecta, is an A-genome diploid (genome formula A₂A₂). From plant morphology, the A-subgenome of amphiploid T. patula is regarded as more likely derived from T. erecta than from T. jaliscensis. In T. jaliscensis X erecta F₂, disk corolla anthocyanin (R = red) from T. jaliscensis segregated as a simple dominant over the absence of anthocyanin from T. erecta. A chlorophyll defect was determined by duplicate factor recessives. Tubular ray flowers (tu = tubular) segregated as a simple recessive to normal flat rays in the interspecific F₂ and in T. erecta.