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J J Bonner

Publications and source records attributed to J J Bonner.

At least 37 records · Page 2Linked to original sources
PubMed1985

Clonal analysis of two mutations in the large subunit of RNA polymerase II of Drosophila.

Two mutations in the gene, RpII215, were analyzed to determine their effects on cell differentiation and proliferation. The mutations differ in that one, RpII215ts (ts), only displays a conditional recessive lethality, while the other, RpII215Ubl (Ubl), is a recessive lethal mutation that also displays a dominant mutant phenotype similar to that caused by the mutation Ultrabithorax (Ubx). Ubl causes a partial transformation of the haltere into a wing; however, this transformation is more complete in flies carrying both Ubl and Ubx. The present study shows that patches of Ubl/-tissue in gynandromorphs are morphologically normal. cuticle that has lost the wild-type copy of the RpII215 locus fails to show a haltere to wing transformation, nor does it show the synergistic enhancement of Ubx by Ubl. We conclude that an interaction between the two RpII215 alleles, Ubl and RpII215+, is responsible for the mutant phenotype. Gynandromorphs carrying the ts allele, when raised at permissive temperature, display larger patches of ts/-cuticle than expected, possibly indicating that the proliferation of ts/+ cells is reduced. This might result from an antagonistic interaction between different RpII215 alleles. Classical negative complementation does not appear to be the cause of the antagonistic interactions described above, as only one RpII215 subunit is thought to be present in an active multimeric polymerase enzyme. We have therefore coined the term 'negative heterosis' to describe the aforementioned interactions. We also observed that the effects of mutationally altered RNA polymerase II on somatic cells are different from its effects on germ cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Mandibular skeletal dysmorphology in micrognathic mice.

The primary manifestations of micrognathia were microglossia, midline fusion of the right and left sides of the mandible, total absence of incisor and molar toothbuds and, in many cases, absence or perhaps premature resorption of Meckel's cartilage. In addition, there was altered osteogenesis as evidenced by disrupted trabecular patterns, as well as an overall dimensional reduction of the mandible both antero-posteriorly and laterally. Strikingly similar results were reported by Johnson (1926), who studied the progeny of x-irradiated mice. How specifically our results correlate with this much earlier work is a matter for further analysis. It seems clear that the critical factor in the development of micrognathia is not so much an abnormal formation of the bony mandible, but a deficiency of tongue development, specifically its intrinsic musculature. Thus, mandibular micrognathia involves not only a dysmorphology of the first branchial arch, but also the mesenchymal cell migration from the occipital somites. Taken together, the picture is one that suggests an underlying cause that may have its inception at a much earlier developmental stage, when ectomesenchymal migration from the region of the neural tube occurs. In any event, we can report confidently that spontaneous micrognathia in prenatal mice is not a simple dimensional reduction of the lower jaw, but a more complex morphological phenomenon.

Animals↗
PubMed1984

Glucocorticoid-induced cleft palate genes in chromosome 17: genetic linkage and mapping analyses.

Genes that influence susceptibility to dexamethasone-induced cleft palate and tentatively designated Dep are linked to the major histocompatibility complex H-2 in chromosome 17 of the mouse. Experiments presented refine the map of genes. The results show two or three Dep loci. The two-locus model maps Dep genes to the class II gene E beta and to the chromosomal region between the S and D genes. The three-locus model maps the Dep genes to the chromosomal regions from the centromere to E beta, from E beta to S, and from D to Pgk-2. Experiments were done by comparing the dexamethasone-induced cleft palate dose response of congenic strains with H-2 haplotypes that are recombinants of H-2a and H-2b. The analysis of genetic linkage between H-2 and Dep was expanded to include reciprocal backcrosses. A maternal factor was found to influence the frequency of dexamethasone-induced cleft palate in the backcross fetuses. The factor's origin is associated with the H-2 haplotype of the outcross mother, so the effect is actually a "grandmother effect" that probably is transmitted horizontally. Finally, the sexes were distributed unevenly between the fetuses with cleft palate in two of the congenic strains. This suggests interaction between the H-2-linked Dep genes and a Dep sex-associated gene that modulates susceptibility to dexamethasone-induced cleft palate.

Alleles↗
PubMed1984

The use of promoter fusions in Drosophila genetics: isolation of mutations affecting the heat shock response.

We have constructed a gene fusion using the promoter of Drosophila hsp70 and the structural gene for Drosophila alcohol dehydrogenase (Adh) and used this construct to transform Adh-deficient flies. In these transformants, Adh is expressed only after heat shock. Like hsp70 itself, this heat-shock-inducible Adh (Adhhs) is induced in a wide variety of tissues. It fails to be induced in primary spermatocytes. Although the tissue distribution of Adh activity is very different from wild type, this does not appear to be deleterious. Indeed, the induction of Adhhs allows flies to survive exposure to ethanol. We have used this latter characteristic to select dominant, trans-acting mutations that alter the response of flies to heat shock.

Alcohol Oxidoreductases↗
PubMed1983

Glucocorticoid-induced cleft palate in the mouse: two major histocompatibility complex, H-2, loci with different mechanisms.

Isolated cleft palate is induced in the progeny of pregnant mice that are given glucocorticoids. The incidence varies among inbred strains and with dose and stage of gestation when the drug is given. One chromosomal region responsible for strain-associated differences in sensitivity is the major histocompatibility complex, H-2. H-2a is associated with susceptibility, H-2b with resistance. There appear to be both maternal and embryonic genetic factors affecting the sensitivity to glucocorticoids. In experiments reported here congenic strains of mice with H-2a, H-2d and H-2k haplotypes on a C57BL/10 genomic background were used. This allowed the determination of the effect on sensitivity by two H-2 subregions; the subregions are H-2K to I-E and I-C to H-2D. Methods included dose-response analysis and reciprocal cross analysis using dexamethasone given on day 12 of pregnancy. Results show that each subregion affects the strain's sensitivity to dexamethasone-induced cleft palate. The regression coefficients for B10.A-H-2a (45.4 +/- 4.13) were different from those for B10.BR-H-2k (67.2 +/- 10.8) and B10.D2-H-2d (70.5 +/- 9.74). The estimated mean arcsine % cleft palate at 160 mg/kg was different for each strain: B10.A-H-2a, 53.1 +/- 2.19; B10.BR-H-2k, 33.1 +/- 2.27; B10.D2-H-2d, 25.0 +/- 2.75. Different patterns of change in sensitivity were observed among the reciprocal crosses. In summary, the H-2K to I-E subregion seemed to influence both maternal and embryonic factors, whereas only embryonic factors were influenced by the I-C to H-2D subregion. These data suggest that the mechanisms affecting glucocorticoid sensitivity which are genetically encoded within each H-2 subregion are different, and there is an interaction between the alleles. The mode of interaction can be either complementation or epistasis.

Animals↗
PubMed1982

Backcross test demonstrates the linkage of glucocorticoid-induced cleft palate susceptibility to H-2.

Data in this report demonstrate a linkage between glucocorticoid-induced cleft palate susceptibility and H-2. B10.A X C57BL/10F1 females were backcrossed to C57BL/10 males. Cleft palate was induced in the BC1 fetuses by giving pregnant females 80 mg/kg of dexamethasone intraperitoneally (IP) on day 12 of gestation. The H-2a/b haplotype was detected on day 18 BC1 fetal spleen cells with an indirect immunofluorescent labeling technique. Fetuses without antigen H-2Kk were H-2b/b . H-2a/b fetuses had a cleft palate frequency of 29%; 11% of the H-2b/b fetuses had cleft palate (P less than .01), demonstrating that the higher susceptibility to cleft palate segregates with the H-2a halotype.

Animals↗
PubMed1982

RNA polymerase II transcribes all of the heat shock induced genes of Drosophila melanogaster.

Heat shock of Drosophila melanogaster induces the transcription of a small number of RNAs. Some of these encode protein products, but not all. We have investigated whether the several induced RNAs are transcribed by RNA polymerase II or by some other RNA polymerase. Immunochemical staining of polytene chromosomes indicates that, on heat shock, RNA polymerase II is relocalized; it "migrates" from previously-active transcription sites to the heat shock induced loci. All heat shock induced puffs show immunochemical staining. Such staining correlates with RNA polymerase II activity as judged by the sensitivity of RNA synthesis at these sites to low concentrations of alpha-amanitin. Thus the protein-coding and non-protein-coding heat shock-induced RNAs are transcribed by this polymerase specifically. We have also identified several non-puffed chromosomal sites at which RNA synthesis is induced by heat shock.

Animals↗
PubMed1982

Cleft palate susceptibility maps in two H-2 subregions, H-2K to I-B and G to H-2D.

Data presented here defines the map of H-2 associated genes which affect the glucocorticoid-induced cleft palate frequency to the regions H-2K to I-B and G to H-2D. This was done by observing in four congenic strains the frequency of cleft palate induced by 160 mg/kg of dexamethasone administered to pregnant females on day 12 of gestation. The strains used were B10.A/Sg.Sn, C57BL/10Sn, B10.A (5R)/SgSn and B10.A(18R)/Sg. Additionally the cleft palate frequency was observed in a large number of litters from saline-treated pregnant females. The cleft palate frequency in this control was very low and the rank of strains was the same as for the glucocorticoid-induced cleft-palate frequency. This observation suggests that the induced cleft palate frequency reflects the spontaneous occurrence of isolated cleft palate in these strains.

Animals↗