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41.
42.
Donald C. Morizot Jeffrey A. Greenspan Michael J. Siciliano 《Biochemical genetics》1983,21(9-10):1041-1049
Electrophoretic variation ascribable to three protein-coding loci, coding for glutamine synthetase (GS), uridine monophosphate kinase (UMPK), and transferrin (Tf), was observed in three species of fish of the genus Xiphophorus. Electrophoretic patterns in interspecific F1 hybrid heterozygotes suggested monomeric subunit structures of UMPK and Tf and a multimeric structure of undetermined subunit number of GS. Linkage analyses in backcross hybrids indicated a recombination map of GS-0%-Tf-10.8%-UMPK. This group (designated Xiphophorus linkage group VI) was shown to assort independently from the 14 enzyme loci assigned to linkage groups I-V and from 19 other informative markers within the limits of the data. 相似文献
43.
Jeffrey R. Bloomquist David M. Soderlund Douglas C. Knipple 《Archives of insect biochemistry and physiology》1989,10(4):293-302
Resistance to pyrethroid insecticides and dichlorodiphenyltrichloroethane (DDT) was investigated in the napts (no action potential, temperature sensitive) mutant of Drosophila melanogaster. In surface contact bioassays, the napts strain showed threefold resistance to deltamethrin at the LC50 level when compared to susceptible Canton-S flies. Cross-resistance was also observed to DDT and the pyrethroids NRDC 157 [3-phenoxybenzyl [1R,cis]-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylate], fenfluthrin, and MTI-800 [1-(3-phenoxy-4-fluorophenyl)-4-(4-ethoxyphenyl)-4-methylpentane]. The onset of intoxication by pyrethroids in napts flies was markedly delayed, a finding that is consistent with the existence of a resistance mechanism involving reduced neuronal sensitivity. Resistance at the level of the nerve was confirmed by electrophysiological recordings of spontaneous and evoked activity in the dorsolongitudinal flight muscles of poisoned flies. Preparations from napts insects treated with fenfluthrin displayed longer latencies to the appearance of spontaneous activity and also an absence or reduction in burst discharges compared to equivalent preparations from susceptible individuals. These results are discussed in light of competing hypotheses concerning the mechanism underlying knockdown resistance and reduced nerve sensitivity in insects. 相似文献
44.
Joseph G. Major Jr. Melinda E. Wales John E. Houghton Julie A. Maley Jeffrey N. Davidson James R. Wild 《Journal of molecular evolution》1989,28(5):442-450
Summary Aspartate transcarbamoylase (ATCase, EC 2.1.3.2) is the first unique enzyme common to de novo pyrimidine biosynthesis and
is involved in a variety of structural patterns in different organisms. InEscherichia coli, ATCase is a functionally independent, oligomeric enzyme; in hamster, it is part of a trifunctional protein complex, designated
CAD, that includes the preceding and subsequent enzymes of the biosynthetic pathway (carbamoyl phosphate synthetase and dihydroorotase).
The complete complementary DNA (cDNA) nucleotide sequence of the ATCase-encoding portion of the hamster CAD gene is reported
here. A comparison of the deduced amino acid sequences of the hamster andE. coli catalytic peptides revealed an overall 44% amino acid similarity, substantial conservation of predicted secondary structure,
and complete conservation of all the amino acids implicated in the active site of theE. coli enzyme. These observations led to the construction of a functional hybrid ATCase formed by intragenic fusion based on the
known tertiary structure of the bacterial enzyme. In this fusion, the amino terminal half (the “polar domain”) of the fusion
protein was provided by a hamster ATCase cDNA subclone, and the carboxyl terminal portion (the “equatorial domain”) was derived
from a clonedpyrBI operon ofE. coli K-12. The recombinant plasmid bearing the hybrid ATCase was shown to satisfy growth requirements of transformedE. coli pyrB
− cells. The functionality of thisE. coli-hamster hybrid enzyme confirms conservation of essential structure-function relationships between evolutionarily distant
and structurally divergent ATCases. 相似文献
45.
46.
47.
Alison H. Hammond Michael J. Garle Jeffrey R. Fry 《Journal of biochemical and molecular toxicology》1995,10(5):265-273
Precocene II was more toxic in 24 hour cultures than in 72 hour cultures of rat hepatocytes. In 24 hour cultures, there was no observable toxicity at 75 μM precocene II after exposure for 6 hours, but after 24 hours, 65% of the cells were dead. In contrast, although 794 μM killed 50% of the cells in the 72 hour cultures after a 24 hour exposure, 1 mM killed 96% of the cells within 6 hours. In both 24 and 72 hour cultures, cell death was preceded by a rapid, early loss of mitochondrial membrane potential, followed by decreases in glutathione, reduced pyridine nucleotide status, and plasma membrane Na+/K+-ATPase activity. There was also a rapid loss of ATP in the 72 hour cultures but not in the 24 hour cultures; therefore, onset of cell death may be closely linked to loss of ATP. Inhibition of cytochrome P-450 prevented the toxicity, and partially protected against the loss of membrane potential and glutathione, in 24 hour cultures but was ineffective in 72 hour cultures. Therefore, in addition to depletion of glutathione, precocene II appears to damage mitochondria and plasma membrane functions and can do so by more than one pathway. © 1996 John Wiley & Sons, Inc. 相似文献
48.
Desmond R. Jimenez Jeffrey P. Shapiro Raymond K. Yokomi 《Entomologia Experimentalis et Applicata》1994,70(2):143-152
This study was conducted to evaluate the effect of two different biotypes of the sweetpotato whitefly,Bemisia tabaci (Gennadius), on the induction of squash silverleaf (SSL), and to determine if double-stranded RNA (dsRNA) occurs in geographically
remote populations of the two biotypes. Recently collected B-biotype whiteflies from Florida, Arizona, Mississippi, and Texas
(SPW-B) all contained a 7.0 kb dsRNA molecule. Kb dsRNA molecule. Laboratory colonies of A-biotype whiteflies that were originally
collected in 1981 from cotton in Arizona and California did not contain the 7.0 Kb dsRNA. When the two biotypes were compared
only the SPW-B induced rapid onset, grade 5, SSL. DsRNA similar to that found in adult SPW-B was concentrated in whitefly
nymphs, but host plant leaf tissue did not contain any consistent dsRNA molecules. SPW-A only induced low-grade SSL and progeny
of SPW-A that were fed on pumpkin plants displaying SSL did not acquire the ability to express dsRNA or induce SSL. Our data
suggest that dsRNA is not directly involved in the induction of SSL and that SSL is a host-specific response, to a feeding
injury induced by B-biotype whiteflies. The origin and source of the 7.0 Kb dsRNA molecule remains enigmatic but its expression
is constant in the whitefly biotype that is responsible for the induction of SSL and several other plant disorders in the
U.S. 相似文献
49.
Catarina E. Hioe Denise M. McKinney Jeffrey A. Frelinger Minnie McMillan 《Immunogenetics》1994,40(3):222-229
In order to investigate the role of residues inside and outside the peptide binding cleft of the L2 molecule in peptide presentation to cytotoxic T lymphocytes (CTL), we constructed a series of point mutations in the L
d
gene. We determined the effects of the mutations in the Ld molecule on the binding and recognition of an Ld-restricted CTL epitope derived from the nucleoprotein (NP) of the lymphocytic phoriomeningitis virus (LCMV). Each of the mutations within the Ld peptide binding cleft resulted in a complete loss of CTL recognition. Addition of the LCMV NP peptide to cells expressing these mutants did not increase surface Ld expression, suggesting that the mutations altered peptide binding. Mutations involving pockets D and E within the cleft affected LCMV peptide binding and recognition as drastically as those in pocket B, which was predicted to interact with a main anchor residue of the peptide. In striking contrast, the mutations located outside the cleft did not change either recognition or binding. These results demonstrate that the Ld residues in the peptide binding cleft are the main determinants dictating LCMV NP peptide binding, and that the residues in each of the pockets within the cleft play a role in this interaction. Surprisingly, one mutation outside the peptide binding cleft, T92S, abrogated CTL lysis of target cells treated with the LCMV NP peptide, but not virus-infected cells. These data show that this mutation selectively altered the presentation of the LCMV NP peptide introduced to the cell exogenously, but not endogenously. This implies that the pathway by which peptides associate with class I molecules within the cell differs from that of exogenous peptide binding. 相似文献
50.
A genomic clone containing the gl1–2 allele has been isolated and sequenced. The predicted amino acid sequence of the gl1–2 protein is identical to that of the GL1-Col allele up to position 201. At this point in the coding region of gl1–2 there is a deletion relative to the wild-type sequence that results in an in-frame stop codon at position 202. This deletion removes 27 amino acid residues, including a highly negatively charged region, from the predicted gl1–2 polypeptide. The loss of this negatively charged carboxy-terminal region from the gl1–2 product is most likely the cause of the partial loss of gene activity which results in a reduction in leaf trichome initiation. 相似文献