高粱对丝黑穗病的抗性及遗传研究

1981—1985年在人工接种的条件下,对1239份高粱品种资源,进行了抗丝黑穗病性鉴定。与此同时,用17个抗性不同的品种系,按照不完全双列杂交设计,进行了高粱对丝黑穗病的抗性遗传研究。结果表明,高粱对丝黑穗病的抗性遗传方式因品种而异。有的品种系具数量性状遗传特点,有的则具有质量性状遗传特点。抗病性属数量性状遗传的品种系,其抗性主要是受加性基因控制。     

+G_z暴露时,家兔心率和心水平动脉压关系的研究

在动物离心机上测定了7只轻度麻醉家免暴露于+G_Z时心、眼水平动脉压和心率的变化。+G_Z作用5-12s时、心水平动脉压(HABP)降至最低水平,然后开始代偿性回升。当+G_Z增大到一定值时,于加速度达峰值后,HABP降为0 mmHg、并在峰值后5.5±1.7s降到最大负值,继之代偿性升为正值,并常再度降为负值。我们称HABP的这种变化状态为“临界状态”。+G_Z暴露时,心率以两种型式发生改变:第一种,随着G值增大,心率发生不同程度增快,当加速度达某一G值时,心率突然减慢至2次/秒左右;第二种,当G值≥3时,在暴露过程中,心率逐渐减慢,并在某一G值,心率减慢到2次/秒左右。心率和HABP关系密切。当HABP达临界状态时,心率减慢至2次/秒左右并出现明显节律不整。以心率减慢到2次/秒左右作为家免+G_Z耐力终点是合适的,该指标规律性强,重复性好,实验方法对动物无损伤又易实施。按此标准,测得7只家免的+G_Z耐力为4.85±0.47G。     

Mechanisms of tetracycline and rifampicin resistance inBacteroides fragilis mutants obtained by ionizing radiation

Summary Based on a dose-survival curve, a radiation dose of 3.99 C/kg was used to induce antibiotic-resistant mutants inBacteroides fragilis. Escherichia coli B/r membrane fragments were employed as a reducing agent. Antibiotic-resistant mutants ofB. fragilis were utilized to study the mechanism by which these organisms become resistant to selected chemotherapeutic agents. Decreased accumulation of tetracycline by resistant mutants ofB. fragilis suggests that the resistance to this antibiotic is associated with the outer membrane permeability. There is a marked difference in the inhibitory action of rifampicin on RNA polymerase activity in rifampicin-sensitive and-resistant strains ofB. fragilis. This enzyme is, therefore, the likely target for inhibition of bacterial growth in this anaerobe by rifampicin.     

Resistance ofSpodoptera frugiperda [Lep.: Noctuidae] to a nuclear polyhedrosis virus in the field and laboratory

Median lethal doses (LD₅₀s) of nuclear polyhedrosis virus (NPV) were determined in neonatal offspring ofSpodoptera frugiperda (J. E. Smith) (Sf) larvae captured in southeastern Louisiana in 1981, 1982, and 1984. These LD₅₀s ranged from 1.8 to 16.3 polyhedral inclusion bodies (PIB)/insect. The LD₅₀s significantly (P<0.05) increased during the season of 1982 but had no pattern in 1981 or 1984. However, the Sf populations increased in heterogeneity of response to the NPV during all 3 years. The LD₅₀ increased from 4.1 to 18.7 PIB/insect in a Sf laboratory colony exposed to the NPV LD₈₀ for 7 generations, whereas in a control colony not exposed to NPV the LD₅₀ was 5.9 PIB/insect after 7 generations.     

Disturbed lipid metabolism in diabetic coronary vessels

The aim of this study was to clarify whether or not arachidonic acid metabolic disorders are caused by a substrate inavailability and whether such disorders might contribute to circulatory disturbances in the diabetic myocardium. Norepinephrine induced a decrease in the conductivity of both coronary arterial bed and myocardial microcirculation in alloxan-diabetic dogs. It was markedly (p < 0.05) attenuated both by indomethacin and acetylsalicylic acid pretreatments indicating an imbalance among the vasoactive prostanoids in diabetes. TXA₂ release from the diabetic coronary rings was found to be elevated and could be normalized after the blockade of vascular adrenoceptors by phentolamine (p < 0.05). PGIZ synthesis was also enhanced by adrenergic blockade in the diabetic arterial rings. After pretreatment with ^l4C arachidonic acid, in order to measure substrate availability, the arachidonic acid metabolic rate was less in the diabetic coronary arteries than in healthy vessels (p < 0.05). Ten µmol/1 norepinephrine decreased arachidonic acid metabolism in the presence of prelabelled substrate in the diabetic animals, compared to an increase observed in metabolically healthy dogs. Therefore diabetes appears to diminish arachidonic acid metabolism and uptake independent of adrenoceptors and to induce an imbalance between vasoconstrictor and vasodilator cyclooxygenase products, resulting in elevated TXA₂ release controlled by adrenergic mechanisms which may contribute to an impairment in myocardial microcirculation.Abbreviations 6-oxo-PGF₁ 6-oxo prostaglandin F₁ - HPLC High Pressure Liquid Chromatograph - LAD Left Anterior Descending (coronary artery) - PGI₂ Prostacyclin - TXA₂ Thromboxane     

Insertional inactivation of a gene which controls expression of vancomycin resistance on plasmid pHKK100

Expression of inducible high level vancomycin resistance (Vmr) in enterococci appears to require other plasmid-encoded genes in addition to the previously described structural genes vanA and vanH. Tn917 mutagenesis was used to identify such a region in the Vmr plasmid pHKK100. Insertional inactivation of a 693-bp open reading frame upstream from vanH resulted in complete loss of Vmr. This putative 26,642-Da protein has been designated VanR.     

Construction of a new universal vector for insertional mutagenesis by homologous recombination

We describe here the construction of a vector (pSSC-9) which can be used for the insertional mutagenesis of any gene for which genomic sequences have been cloned. This vector contains a neomycin-resistance-encoding gene (neo^R) which is driven by a modified thymidine kinase (tk) promoter for positive selection. Flanking neo^R are two tk genes driven by their own promoters for negative selection of nonhomologous insertions. The neo^R and tk cassettes are separated by four unique cloning sites on the right-hand side of the neo^R cassette and three unique sites on the left-hand side. The vector also includes two SfiI sites, one on each side of the tk cassettes, for the excision of the cloned genomic DNA fragments along with the selectable markers. Electroporation of pSSC-9 into mouse embryonic stem (ES) cells and cultured diploid mouse adrenal Y-1 cells conferred resistance to G418 and sensitivity to ganciclovir in both cell lines. These results illustrate the expression of the positive and negative selectable markers in two different cell lines and thus suggest that the vector could be used in ES cells, as well as in cultured somatic cells.     

Reduced neuronal sensitivity to dieldrin and picrotoxinin in a cyclodiene-resistant strain of Drosophila melanogaster (Meigen).

Toxicological and neurophysiological studies were performed to characterize the resistance mechanism in a cyclodiene-resistant strain of Drosophila melanogaster (Maryland strain). Dieldrin had an LC50 of 0.058 ppm against the larvae of susceptible D. melanogaster (Oregon-R wild type) when formulated in the rearing media. The LC50 of the resistant Maryland strain was 10.8 ppm, giving a resistance ratio (LC50-Maryland/LC50-susceptible) of 186-fold. Suction electrode recordings were made from peripheral nerves of the larval central nervous system to test whether reduced nerve sensitivity played any role in the observed resistance. In susceptible preparations (n = 5), inhibition of nerve firing by 1 mM gamma-aminobutyric acid (GABA) was effectively antagonized within 3-10 min by 10 microM dieldrin. In contrast, 30 min incubations with 10 microM dieldrin had no effect on preparations from cyclodiene-resistant individuals (n = 5). Similarly, 10 microM picrotoxinin blocked GABA-dependent inhibition in susceptible nerve preparations (n = 3). In recordings from resistant insects (n = 4), picrotoxinin displayed either weak antagonism of GABA or hyperexcitation indistinguishable from susceptible preparations. These results demonstrate that cyclodiene resistance in the Maryland strain of D. melanogaster 1) is expressed in immature stages, 2) is present at the level of the nerve, and 3) extends to picrotoxinin, albeit at a reduced level compared with dieldrin. The possible role of an altered GABA receptor in this resistance is discussed.     

Organisation and functions of the actV A region of the actinorhodin biosynthetic gene cluster of Streptomyces coelicolor

Summary Sequence analysis of the actVA region of the actinorhodin biosynthetic gene cluster of Streptomyces coelicolor revealed a succession of six open reading frames (ORFs), all running in the same direction and extending over 5.32 kb. The protein product of actVA-ORF1 strongly resembles that of another gene, elsewhere in the act cluster (actII-ORF2), which codes for a trans-membrane protein previously implicated in actinorhodin export from the mycelium. This suggests that the two gene products may co-operate in actinorhodin export, perhaps being sufficient for self-protection of the organism against suicide. At least four of the other five ORFs are implicated in the control of the C-6 and C-8 ring-hydroxylation reactions, lacking in actVA mutants, that occur at middle to late stages in the actinorhodin biosynthetic pathway. This conclusion was reached by genetic mapping of actVA mutants to actVA-ORF3 and-ORF5 (and perhaps -ORF4), and by the finding of strong resemblances between the protein products of actVA-ORF2 and -ORF6 and the products of genes of the oxytetracycline or tetracenomycin gene clusters that have been implicated in ring-hydroxylation reactions in the biosynthesis of these other aromatic polyketide antibiotics.     

Recombination at the Rp1 locus of maize.

Summary The Rp1 locus of maize determines resistance to races of the maize rust fungus (Puccinia sorghi). Restriction fragment length polymorphism markers that closely flank Rp1 were mapped and used to study the genetic fine structure and role of recombination in the instability of this locus. Susceptible progeny, lacking the resistance of either parent, were obtained from test cross progeny of several Rp1 heterozygotes. These susceptible progeny usually had non-parental genotypes at flanking marker loci, thereby verifying their recombinational origin. Seven of eight Rp1 alleles (or genes) studied were clustered within about 0.2 map units of each other. Rpl ^G, however, mapped from 1–3 map units distal to other Rp1 alleles. Rp5 also mapped distally to most Rp1 alleles. Other aspects of recombination at Rp1 suggested that some alleles carry duplicated sequences, that mispairing can occur, and that unequal crossing-over may be a common phenomenon in this region; susceptible progeny from an Rp1 ^A homozygote had recombinant flanking marker genotypes, and susceptible progeny from an Rp1 ^DlRp1 ^F heterozygote showed both possible nonparental flanking marker genotypes.