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Biomedical subjects

M Potter

Publications and source records attributed to M Potter.

At least 217 records · Page 12Linked to original sources
PubMed1985

Genetic control of systemic Leishmania major infections: dissociation of intrahepatic amastigote replication from control by the Lsh gene.

Systemic disease induced by Leishmania major was estimated by microscopic examination of liver impression smears and determination of numbers of intrahepatic amastigotes in intravenously or subcutaneously infected inbred, hybrid, and congenic mice. The distribution of susceptible phenotypes among these mice, particularly the susceptibility of a strain congenic for Lshr, strongly suggested that Lsh, a gene which controls intrahepatic replication of Leishmania donovani, does not influence systemic disease by L. major.

Animals↗
PubMed1984

Crystalline monoclonal antibody Fabs complexed to hen egg white lysozyme.

The Fab of a monoclonal anti-lysozyme antibody (HyHEL-10) has been crystallized as the free Fab and as the Fab-antigen complex. Crystals have also been grown of the antigen complex of the Fab of another monoclonal anti-lysozyme antibody (HyHEL-9), which recognizes a different binding surface of lysozyme. All three crystals diffract to at least 3 A resolution and are suitable for X-ray diffraction studies.

Animals↗
PubMed1984

Activation of the c-myb locus by viral insertional mutagenesis in plasmacytoid lymphosarcomas.

Rearrangement in the c-myb locus of each of four independently derived BALB/c plasmacytoid lymphosarcoma (ABPL's) is due to the insertion of a defective Moloney murine leukemia virus (M-MuLV) into a 1.5-kilobase-pair stretch of cellular DNA at the 5' end of the v-myb-related sequences. This retroviral insertion is associated with abnormal transcription of myb sequences and probably represents a step in the neoplastic transformation of ABPL cells.

Animals↗
PubMed1984

Effect of MuLV-related genes on plasmacytomagenesis in BALB/c mice.

The role of spreading somatic cell infections with ecotropic MuLV viruses in the induction of plasmacytomas in BALB/cAN pi mice was determined by constructing congenic mice that lacked the gene locus Cv that codes for ecotropic virus. DBA/2 mice that lack Cv on chromosome (chr) 5 carry a closely linked gene Rmcfr that determines resistance to infection with mink cell focus-forming viruses (MCF). Rmcfr was retrogressively back-crossed onto BALB/c for six successive generations to produce N6 mice. N6 mice were mated to each other to produce BALB/c.DBA/2 Rmvfr/Rmcfr homozygotes. This stock of mice lacked Cv, as demonstrated by DNA hybridization and were as fully susceptible to developing plasmacytomas as the parental BALB/c. A second congenic stock BALB/c.DBA/2 Rmcfr/Rmcfr Fv-1n/Fv-1n was also developed, but the mice of this stock showed a reduced incidence of plasmacytomas, as did BALB/c.DBA/2 Fv-1n/Fv-1n mice. These findings indicated Fv-1 or a gene closely linked to it conferred partial resistance to plasmacytomagenesis. In constructing the BALB/c.DBA/2 Fv-1n/Fv-1n stock, a "control" congenic BALB/c.DBA/2 Fv-1b/Fv-1b was also developed at N6. Surprisingly, this stock carried the Qa2+ trait. These mice were also partially resistant to plasmacytomagenesis, suggesting a gene on chromosome 17 (the location of Qa2) or a gene located elsewhere that regulates Qa2 expression is linked to a gene controlling partial resistance to plasmacytoma development.

Animals↗
PubMed1984

Chromosomal translocations activating myc sequences and transduction of v-abl are critical events in the rapid induction of plasmacytomas by pristane and abelson virus.

Plasmacytomas with short latent periods can be induced in BALB/c mice by a single intraperitoneal (i.p.) injection of 0.5 ml pristane followed 20-40 d later by an injection of Abelson virus. The karyotypes of 18 such tumors were determined; 10 of these had rcpt 12;15, 5 had rcpt 6;15 and 3 had no translocations, but two of these have been shown to have interstitial deletions of chromosome 15. The specific breakpoints were the same as described in pristane-induced plasmacytomas, i.e., at 15D2 /3, 6C2 , and 12F2 . Near diploid karyotypes and trisomy of chromosome 11 were frequently seen. All of the Abelson-plus-pristane-induced plasmacytomas (ABPC) were studied as transplanted tumors, contained integrated v- abl sequences, and actively transcribed v- abl mRNA. All but one of these tumors contained abundant myc RNA transcripts. The shortness of the latent periods of the ABPC suggests that the rcpt 12;15 and rcpt 6;15 occur soon after pristane administration and are present at the time Abelson virus is introduced. In this form of plasmacytomagenesis , activated v- abl genes appear to bypass other genetic changes that require a much longer period of time in pristane plasmacytomagenesis . Nonetheless, the consistent finding of chromosome-15 alterations and abundant myc expression in these plasmacytomas emphasize the apparent need for multiple events even in the genesis of some tumors induced by rapid transforming viruses.

Abelson murine leukemia virus↗
PubMed1984

High resolution banding analysis of the involvement of strain BALB/c- and AKR-derived chromosomes No. 15 in plasmacytoma-specific translocations.

Plasmacytomas were induced in (BALB/c X AKR 6;15) X BALB/c backcross mice where one of the BALB/c-derived chromosomes No. 15 was replaced by the AKR(6;15)-derived Robertsonian 6;15 chromosome. (BALB/c X AKR 6;15)F2 mice that were homozygous for Rb 6;15 were mated to BALB/c mice. Plasmacytomas were induced in the progeny by intraperitoneal injection of pristane. The cytogenetic marker permitted the distinctive identification of the two chromosome 15 homologues, including the distal segment involved in the plasmacytoma-specific translocations. 7 of the 10 plasmacytomas contained the typical t(12;15) translocation. The BALB/c-derived 15 chromosome served as the donor of the translocated segment in six of them. In the seventh, the Rb 6;15 chromosome of the AKR strain was the donor. The remaining three tumors contained the same type of intrachromosomal rearrangement. It arose by the pericentric inversion of the Rb 6;15 chromosome, leading to a variant plasmacytoma-associated rcpt (6;15) translocation. Unlike the usual 6;15 variant that arises by a reciprocal exchange between two separate chromosomes, it was generated by an exchange of the distal segments of a single chromosomal element. High resolution banding analysis of the tumors showed that all translocated breakpoints on chromosomes 15, 12, and 6 were identical with the previously described breakpoints characteristic for the typical 12;15 and the variant 6;15 translocation in murine plasmacytomas. It is known that the distal segment of chromosome 15 carries the c-myc oncogene (23). The PC-associated translocations cut across the 5'-exon of c-myc in the majority of the cases (24,26). The severed oncogene is transposed to the Ig-region on the recipient chromosome. Since the BALB/c strain is highly sensitive to PC-induction, we were interested to examine the question whether its chromosome 15 is preferred as the oncogene donor in AKR X BALB/c backcross mice that carry cytogenetically distinguishable 15 chromosomes. Our results show that this is not the case, since the same segment of the AKR-derived chromosome 15 could also serve in the same capacity. This is in contrast with T cell leukemogenesis where we have previously found that the trisomization-associated duplication of chromosome 15 occurred in a highly asymmetrical fashion, depending on the donor strain of No. 15 (9-11).

Animals↗
PubMed1984

A refined model for the variable domains (Fv) of the J539 beta(1,6)-D-galactan-binding immunoglobulin.

A refined protocol for building a hypothetical model of the J539 Fv is described. Computer programs for positioning amino acid side chains and structure energy minimization [CHARMM program of Brooks et al., J. comp. Chem. 4, 187-217 (1983)] were employed. Computer modeling was accomplished on an Evans and Sutherland picture system which permitted structure visualization in three dimensions. Peptide backbone breaksites were rejoined by monitoring for correct distances and torsion angles. A physical model was then constructed and used as a basis for further refinements such as aligning conformations around remodeled sites, adjusting proline substitutions and optimizing hydrogen-bond-forming potentials. This structure (J539-ADO) was energy minimized and the final coordinates were obtained from the energy-refined model. The resulting hypothetical J539 structure can be compared to the structure of J539 now being determined by X-ray crystallography. The procedures described can be used for other Fv fragments.

Amino Acid Sequence↗
PubMed1984

Hemizygous interstitial deletion of chromosome 15 (band D) in three translocation-negative murine plasmacytomas.

Three murine plasmacytomas that were exceptional in lacking the characteristic (12;15) or (6;15) translocations were studied by G banding and high-resolution banding. One of every two chromosomes 15 (two of four in tetraploid tumors) was shortened in all three tumors. High-resolution banding analysis revealed that this was due to an interstitial deletion in the 15D band region. The two breaks responsible for the deletion have been tentatively localized to the interface of bands D2/3' and within band D2. One of the three plasmacytomas, ABPC45, had a rearranged c-myc gene. All three tumors contained a greater abundance of 2.4-kilobase myc RNA transcripts than normal spleen or thymus. The c-myc gene is located in the 15 D2/3 band region. We suggest that it may have joined the centromeric portion in the deletion plasmacytomas. This transposition may have led to its constitutive activation, as in the more frequent translocation-carrying plasmacytomas.

Animals↗
PubMed1984

Somatic mutation and antibody diversity.

Nucleotide insertions or deletions determine novel amino acid sequences at the VH-D and D-JH junction sites. Since these cannot be predicted by known coding genes, they are regarded as a form of somatic mutagenesis. A second type of somatic mutation in Ig structural genes are the stochastic base substitutions that have now been found in both V region coding sequences and noncoding flanking sequences. It has been proposed that this form of mutagenesis may be related to the gene rearrangement process as well. A third type of mutagenesis has been associated with Ig CH switching. In this case, a higher frequency of substitutions has been observed in VH regions associated with C gamma and C alpha. A mechanism for the origin of this phenomenon is not known. An unexpectedly high rate of mutagenesis affecting Ig V genes has been observed to occur spontaneously in vitro.

Amino Acid Sequence↗
PubMed1984

Polymorphism of C lambda genes and units of duplication in the genus Mus.

The number of Ig C lambda genes in nine geographically widespread species from the four subgenera in the genus Mus was estimated from the number of Bam HI and Eco RI restriction fragments that hybridize under high stringency conditions to cDNA probes of BALB/c inbred mouse origin (Mus musculus domesticus). Three closely related species in the subgenus Mus, M. musculus, M. spretus, and M. spicelegus, show considerable variation in the number of C lambda genes. Estimates of gene numbers in these animals range from two C lambda genes in M. spretus from Puerto Real, Spain to 12 C lambda genes in M. musculus musculus from Studenec, Czechoslovakia. Strains of mice carrying either six or 10 C lambda genes were derived from a single population of M. musculus domesticus from Centreville, MD. The hybridization patterns of mice exhibiting C lambda gene amplification indicate that duplications are of relatively recent origin and probably occurred by reiteration of a DNA segment closely related to the 6.5 kb [C lambda 3 - C lambda 1] unit found in BALB/c inbred mice. Three more distantly related species in the subgenus Mus, and a species representing the Nannomys subgenus all appear to carry only four C lambda genes. DNA of species representing the Coelomys and Pyromys subgenera hybridized weakly to the C lambda cDNA probes, but these animals also have no more than four C lambda genes. Thus, there may be a base number of four C lambda genes in most species in the genus Mus. All inbred strains of mice so far examined also have only four C lambda genes, but no feral M. musculus examined have fewer than six C lambda genes. One explanation of the discrepancy in the number of genes between inbred and feral M. musculus is that C lambda genes were deleted during the process of inbreeding.

Animals↗
PubMed1984

Variation in V lambda genes in the genus Mus.

The complement of Ig V lambda genes in nine species of feral mice representing the four extant subgenera of the genus Mus was examined and compared with that of BALB/c inbred mice. Although all inbred strains examined have two V lambda genes, there is variation in the number of copies of V lambda genes in the wild mice. All feral representatives of M. musculus domesticus, from which inbred strains are derived, have at least three V lambda genes, indicating that a V lambda gene may have been lost during the inbreeding process. At least three V lambda genes are also found in representatives of three other M. musculus subspecies, including the stock of M. musculus musculus "Czech II" shown to have at least 12 C lambda genes. In comparing the complement of V lambda and C lambda genes in these animals, evidence is found that supports a mechanism of lambda gene reiteration involving duplication of a unit containing a V lambda and two C lambda genes. However, the possibility that C lambda gene amplification occurred independent of V lambda gene evolution cannot be ruled out. M. spicelegus and M. spretus, species that are semifertile with M. musculus, have one to three V lambda genes. Species more distantly related to M. musculus, such as M. cookii and M. platythrix, appear to have more (four to six) V lambda genes. Greater V lambda gene heterogeneity is also found in these animals. We propose that the ancestors of the subgenus Mus had more V lambda genes than are seen in modern species and that the paucity of V lambda genes in M. musculus, M. spicelegus, and M. spretus may be the result of V lambda gene deletion events that occurred since the divergence of the ancestor of these three species and those of the distantly related species.

Animals↗
PubMed1984

VL-VH expression by monoclonal antibodies recognizing avian lysozyme.

Seven BALB/c hybridoma antibodies directed against the protein antigen, hen egg-white lysozyme c (HEL), were characterized on the basis of their ability to bind lysozymes from 10 species of birds, and their ability to bind HEL competitively. The hybridomas were separable into three complementation groups based upon competitive interactions. The fine specificities of all antibodies were distinct, but two, HyHEL-8 and HyHEL-10, had very similar and overlapping reactivity patterns. To test the hypothesis that VL-VH pairing correlates with binding specificity, the N-terminal amino acid sequences were determined to identify the VL and VH isotopes (subgroups) of the anti-HEL antibodies. HyHEL-8 and -10 shared the VK23 light chain isotype and nearly identical heavy chains in Kabat subgroup I, whereas the heavy and light chain isotypes of all other antibodies differed from HyHEL-8 and -10 and from each other. The heavy and light chain isotypes expressed by HyHEL-8 and -10 are also expressed by XRPC-25, a DNP-binding myeloma protein that does not bind lysozyme. These results are discussed with respect to the contributions of various genetic sources of structural diversity to antibody functional diversity.

Amino Acid Sequence↗