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Biomedical subjects

P Jolicoeur

Publications and source records attributed to P Jolicoeur.

At least 145 records · Page 8Linked to original sources
PubMed1988

Inability of Kaplan radiation leukemia virus to replicate on mouse fibroblasts is conferred by its long terminal repeat.

The molecularly cloned infectious Kaplan radiation leukemia virus has previously been shown to be unable to replicate on mouse fibroblasts (E. Rassart, M. Shang, Y. Boie, and P. Jolicoeur, J. Virol. 58:96-106, 1986). To map the viral sequences responsible for this, we constructed chimeric viral DNA genomes in vitro with parental cloned infectious viral DNAs from the nonfibrotropic (F-) BL/VL3 V-13 radiation leukemia virus and the fibrotropic (F+) endogenous BALB/c or Moloney murine leukemia viruses (MuLV). Infectious chimeric MuLVs, recovered after transfection of Ti-6 lymphocytes with these recombinant DNAs, were tested for capacity to replicate on mouse fibroblasts in vitro. We found that chimeric MuLVs harboring the long terminal repeat (LTR) of a fibrotropic MuLV replicated well on mouse fibroblasts. Conversely, chimeric MuLVs harboring the LTR of a nonfibrotropic MuLV were restricted on mouse fibroblasts. These results indicate that the LTR of BL/VL3 radiation leukemia virus harbors the primary determinant responsible for its inability to replicate on mouse fibroblasts in vitro. Our results also show that the primary determinant allowing F+ MuLVs (endogenous BALB/c and Moloney MuLVs) to replicate on mouse fibroblasts in vitro resides within the LTR.

Animals↗
PubMed1988

Identification of a common helper provirus integration site in Abelson murine leukemia virus-induced lymphoma DNA.

Abelson murine leukemia virus induces oligoclonal pre-B lymphoma in mice. The expression of the v-abl oncogene in target cells does not appear to be sufficient for tumor induction in several mouse strains, and additional genetic events are thought to be required. We postulated that the helper Moloney murine leukemia virus might induce these events, and its potential role as an insertional mutagen was assessed by the search of a common helper provirus integration site in Abelson murine leukemia virus lymphomas. Molecular cloning of cellular sequences adjacent to Moloney proviruses enabled us to identify a cellular region, designated Ahi-1, which was found occupied by the helper proviruses in 16% of Abelson pre-B-cell lymphomas. All proviruses for which the precise integration site within Ahi-1 could be mapped were found to be in the same orientation. Ahi-1 has been mapped to mouse chromosome 10 and represents a new common proviral integration site. These data suggest that the helper virus contributes to the induction of secondary genetic events which may be important for the development of Abelson murine leukemia virus-induced pre-B-cell lymphoma.

Abelson murine leukemia virus↗
PubMed1988

Cross-sectional growth and decline of human stature and brain weight in 19th-century Germany.

A new six-parameter two-phase nonlinear growth and decline model is fitted to cross-sectional data on human stature and brain weight obtained from autopsies in Germany at the end of the 19th century. Brain growth may have ended at a total age of approximately seven years, much younger than estimated in previous studies. Earlier statistical approaches may not have pinpointed the beginning of the plateau. The decline of stature was slight and is weakly significant. The decline of brain weight was stronger but occurred mostly after sixty years of age. Secular increase may have been unimportant from 1820 to 1900.

Adolescent↗
PubMed1988

Asymptotic growth and complex allometry of the brain and body in the white rat.

A new four-parameter version of Pütter's growth curve (Pütter, 1920) is obtained by replacing time by a smooth non-negative function which incorporates an initial delay. Fitted through constrained iteratively-reweighted multiplicative least-squares, this curve provides an accurate description of asymptotic growth and complex allometry of brain weight and body length and weight in a cross-sectional sample of forty-four male white rats.

Animals↗
PubMed1988

A lifetime asymptotic growth curve for human height.

A new seven-parameter asymptotic growth curve has been applied to longitudinal data on the height of 13 boys and 14 girls from 1 month to 19 years of age. The residual sums of squares with this new curve were 7.5 times lower on the average than with the currently-used five-parameter curve No. 1 of Preece and Baines (1978, Annals of Human Biology 5, 1-24) and 2.4 times lower than with the recent six-parameter curve of Shohoji and Sasaki (1987, Growth 51, 432-450). The new curve is expressed with respect to total age, passes through the origin, and fits infants as satisfactorily as older children.

Adolescent↗
PubMed1988

Postnatal brain growth and allometry in the rabbit Oryctolagus cuniculus.

A new four-parameter version of Pütter's growth curve (Pütter, 1920) recently developed by Jolicoeur and Pirlot (1988) is applied to cross-sectional data on brain and body weight in 66 male rabbits (Oryctolagus cuniculus) ranging up to one year in postnatal age. Apart from the olfactory bulb, in which there appears to be no initial delay, the estimated initial delays range from 21.7 days (after fertilization) for the cerebellum to 29.9 days for the cerebrum, which suggests that the weight of most regions of the brain, as well as body weight, start increasing rapidly only toward the end of pregnancy (30 days on the average). These initial delays may be related to the fact that rabbits are born very small, naked, blind, and helpless. Expressed on log-log scales, bivariate allometric trajectories have very diverse shapes, including approximate straight lines, curves possessing a single upward or downward convexity, and even sigmoid or inverted sigmoid curves. It seem doubtful whether, if age were unknown, a reasonably simple mathematical function could possess enough flexibility to describe all of these kinds of relationships satisfactorily.

Aging↗
PubMed1987

Revertants of v-fos-transformed fibroblasts have mutations in cellular genes essential for transformation by other oncogenes.

Morphologic revertants of FBJ murine sarcoma virus (v-fos)-transformed rat-1 fibroblasts were isolated using a novel selection procedure based on prolonged retention of rhodamine 123 within mitochondria of v-fos-transformed versus normal fibroblasts. Two classes of revertants were isolated: class I revertants have sustained mutations in cellular genes, and a class II revertant has a nonfunctional v-fos provirus. Somatic-cell hybridization studies suggested that the revertant phenotype was recessive to the transformed phenotype. Class I revertants were also resistant to retransformation by v-gag-fos-fox, v-Ha-ras, v-abl, and v-mos, but could be retransformed by the trk oncogene and polyoma virus middle T antigen. These results suggest that the class I revertants sustained mutations in one or more cellular genes essential for transformation by some, but not all, oncogenes. Our data suggest the existence of common biochemical pathways for transformation.

Animals↗
PubMed1987

Additivity and interaction between size ratio and response category in the comparison of size-discrepant shapes.

In Experiment 1, subjects made same-different judgments to pairs of shapes that could differ (irrelevantly) in size and in which different pairs combined distinct shapes. Size discrepancy had an effect both on same and different responses. However, the effect on different responses was not monotonic across size discrepancies. It is argued that this nonmonotonicity was produced by a form of bias acting to slow different responses for same-sized pairs. Consistent with the proposed bias account, the nonmonotonic size-discrepancy effect on different trials was eliminated in Experiment 2, in which trials were blocked by size ratio. In Experiment 3, subjects performed a task similar to that in Experiments 1 and 2. However, additional visual information was added inside the bounding contour of the shapes, and this information was either the same or different across shapes. The match between within-contour information across shapes (whether same or different) was varied orthogonally with whether the bounding contours of the shapes were the same or different. In this experiment subjects decided whether the bounding contours of the shapes were the same or different, while ignoring the added information within the contours. When the added information matched across the two shapes, same responses were facilitated relative to when the added information mismatched. The converse occurred for different responses. This effect was more pronounced when the shapes were shown at the same size than when the shapes were at different sizes. In general, the results suggest that (a) size discrepancy affects some perceptual operations that are preliminary to shape matching, and (b) bias mechanisms can play an important role in shape-matching experiments in which the shapes can be shown in different sizes. The interaction of two processes--size scaling and bias--can account for these and hitherto contradictory results in the literature.

Form Perception↗
PubMed1987

Important role of the long terminal repeat of the helper Moloney murine leukemia virus in Abelson virus-induced lymphoma.

The helper virus has been shown to play a critical role in the development of lymphoma induced by the defective Abelson murine leukemia virus (A-MuLV). Indeed, A-MuLV pseudotyped with some viruses, such as the Moloney MuLV, has been shown to be highly lymphogenic, whereas A-MuLV pseudotyped with other viruses, such as the BALB/c endogenous N-tropic MuLV, has been shown to be devoid of lymphogenic potential (N. Rosenberg and D. Baltimore, J. Exp. Med. 147:1126-1141, 1978; C. D. Scher, J. Exp. Med. 147: 1044-1053, 1978). To map the viral DNA sequences encoding the determinant of the lymphogenic potential of Moloney MuLV when complexed with A-MuLV, we constructed chimeric helper viral DNA genomes in vitro between parental cloned infectious viral DNA genomes from Moloney MuLV and from BALB/c endogenous N-tropic MuLV. Chimeric helper MuLVs, recovered after transfection of NIH 3T3 cells were used to rescue A-MuLV, and the pseudotypes were inoculated into newborn NIH Swiss, CD-1, and SWR/J mice to test their lymphogenic potential. We found that a 0.44-kilobase-pair PstI-KpnI long terminal repeat-containing fragment from the Moloney MuLV was sufficient to confer some, but not complete, lymphogenic potential to a chimeric virus (p7M2) in NIH Swiss and SWR/J mice, but not in CD-1 mice. The addition of the 3'-end env sequences (comprising the carboxy terminus of gp70 and all p15E) to the U3 long terminal repeat sequences restored the full lymphogenic potential of the Moloney MuLV. Our data indicate that the 3'-end sequences of the helper Moloney MuLV are somehow involved in the development of lymphoma induced by A-MuLV. The same sequences have previously been found to harbor the determinant of leukemogenicity and of disease specificity of Moloney MuLV when inoculated alone.

Abelson murine leukemia virus↗
PubMed1987

Identification of a new common provirus integration site in gross passage A murine leukemia virus-induced mouse thymoma DNA.

The Gross passage A murine leukemia virus (MuLV) induced T-cell leukemia of clonal (or oligoclonal) origin in inoculated mice. To study the role of the integrated proviruses in these tumor cells, we cloned several newly integrated proviruses (with their flanking cellular sequences) from a single tumor in procaryotic vectors. With each of the five clones obtained, a probe was prepared from the cellular sequences flanking the provirus. With one such probe (SS8), we screened several Gross passage A MuLV-induced SIM.S mouse tumor DNAs and found that, in 11 of 40 tumors, a provirus was integrated into a common region designated Gin-1. A 26-kilobase-pair sequence of Gin-1 was cloned from two lambda libraries, and a restriction map was derived. All proviruses were integrated as a cluster in the same orientation within a 5-kilobase-pair region of Gin-1, and most of them had a recombinant structure of the mink cell focus-forming virus type. The frequency of Gin-1 occupancy by provirus was much lower in thymoma induced by other strains of MuLV in other mouse strains. Using somatic-cell hybrid DNAs, we mapped Gin-1 on mouse chromosome 19. Gin-1 was not homologous to 16 known oncogenes and was distinct from the other common regions for provirus integration previously described. Therefore, Gin-1 appears to represent a new common provirus integration region. The integration of a provirus within Gin-1 might be an important event leading to T-cell transformation, and the Gin-1 region might harbor sequences which are involved in tumor development.

AKR murine leukemia virus↗
PubMed1986

Studies on emerging radiation leukemia virus variants in C57BL/Ka mice.

To analyze the emergence of radiation leukemia virus (RadLV) variants in primary X-ray-induced C57BL/Ka thymoma and to identify the virus responsible for the very high leukemogenic potential of passaged Kaplan strain BL/VL3 preparation, we cloned several primary and passaged ecotropic RadLV infectious genomes. By restriction analysis, we found that BL/VL3 cells harbor three related but different ecotropic RadLVs. Their restriction map differs significantly from those of primary RadLVs. Hybridization analysis also indicated that BL/VL3 and primary RadLVs differ in their p15E and long terminal repeat (LTR) regions. As compared with the LTR sequence of the putative parental endogenous ecotropic provirus, the LTR sequence of primary weakly leukemogenic RadLV has only one change, a C-rich sequence, generating a 6-base-pair direct repeat just in front of the promotor. The LTR of the primary nonleukemogenic RadLV only showed few base changes, mainly clustered in R and U5. The LTR from a moderately leukemogenic passaged BL/VL3 RadLV had conserved the C-rich sequence and acquired a 43-base-pair direct repeat in U3 and several other point mutations, small insertions, and deletions scattered in U3, R, and U5. All cloned primary RadLVs were fibrotropic, and some were weakly leukemogenic. All cloned BL/VL3 RadLVs were thymotropic and nonfibrotropic. The block of their replication was found to be after the synthesis of unintegrated linear and supercoiled viral DNA. Most of the BL/VL3 RadLVs were moderately leukemogenic, and one (V-13) was highly leukemogenic, being as virulent as the Moloney strain. We propose a model for the emergence of the RadLV variants and show that the virus responsible for the high leukemogenic potential of BL/VL3 preparation is a nondefective, ecotropic, lymphotropic, nonfibrotropic, unique retrovirus which most likely arose from a parental primary RadLV similar to those studied here.

Animals↗
PubMed1986

Cas-Br-E murine leukemia virus: sequencing of the paralytogenic region of its genome and derivation of specific probes to study its origin and the structure of its recombinant genomes in leukemic tissues.

The ecotropic Cas-Br-E murine leukemia virus (MuLV) and its molecularly cloned derivative pBR-NE-8 MuLV are capable of inducing hind-limb paralysis and leukemia after inoculation into susceptible mice. T1 oligonucleotide fingerprinting, molecular hybridization, and restriction enzyme analysis previously showed that the env gene of Cas-Br-E MuLV diverged the most from that of other ecotropic MuLVs. To analyze proviruses in leukemic tissues, we derived DNA probes specific to Cas-Br-E sequences: two from the env region and one from the U3 long terminal repeat. With these probes, we found that this virus induced clonal (or oligoclonal) tumors and we documented the presence of typical mink cell focus-forming-type proviruses in leukemic tissues and the possible presence of other recombinant MuLV proviruses. Since the region harboring the determinant of paralysis was mapped within the pol-env region of the virus (L. DesGroseillers, M. Barrette, and P. Jolicoeur, J. Virol. 52:356-363, 1984), we performed the complete nucleotide sequence of this region covering the 3' end of the genome. We compared the deduced amino acid sequences of the pol carboxy-terminal domain and of the env gene products with those of other nonparalytogenic, ecotropic, and mink cell focus-forming MuLVs. This amino acid comparison revealed that this part of the pol gene product and the p15E diverged very little from homologous proteins of other MuLVs. However, the Cas-Br-E gp70 sequence was found to be quite divergent from that of other MuLVs, and the amino acid changes were distributed all along the protein. Therefore, gp70 remains the best candidate for harboring the determinant of paralysis.

Amino Acid Sequence↗
PubMed1986

Proviral integration site Mis-1 in rat thymomas corresponds to the pvt-1 translocation breakpoint in murine plasmacytomas.

Two loci independently implicated in T-and B-lymphocyte neoplasia are shown to be equivalent. The Mis-1 locus is a common proviral integration site in retrovirally induced rat T lymphomas, while the pvt-1 locus on murine chromosome 15 frequently translocates to the kappa locus in plasmacytomas bearing 6;15 translocations. By comparing cloned sequences, we show that pvt-1 is the murine homolog of Mis-1.

Animals↗