E. Peter Volpe
Tulane University
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Archive | 1971
Maria Luiza Beçak; Willy Beçak; Franklin L. Roberts; Robert N. Shoffner; E. Peter Volpe; Kurt Benirschke; T. C. Hsu
The materials for the karyograms were prepared from feather pulp and embryonic tissue of coturnix quail secured through the courtesy of Dr. Hans Abplanalp, University of California, Davis. This colony originated from Japan. This species is one of the few among the birds so far described that have metacentric or submetacentric chromosomes recognizable to about chromosome size twenty.
Science | 1973
James B. Turpen; E. Peter Volpe; Nicholas Cohen
Reciprocal transplantation of undifferentiated thymic primordia between diploid and triploid chromosomally marked frog embryos has revealed that thymic lymphocytes are ontogenically derived from elements of the thymic primordium rather than from blood-borne stem cells that migrated into the developing organ. Virtually all the lymphocytes in the spleen, kidneys, and bone marrow of adult frogs are descendants of these original thymic stem lymphocytes.
Cell and Tissue Research | 1972
Sherill K. Curtis; E. Peter Volpe; Ronald R. Cowden
SummaryA study of the ultrastructure of the developing thymus of the leopard frog (Rana pipiens) revealed that the thymus had undergone all of the major changes which would persist through larval life and metamorphosis by the time that the animals had reached larval stage IV of Taylor and Kollros (1946). These changes included development of an outer, lymphoid cortical region and an inner, essentially nonlymphoid medulla; mitotic activity among lymphoid cell precursors and the formation of the first small lymphocytes; development of complex cysts containing PAS-positive material and the appearance of other signs of secretory activity among epithelial cells of the medulla; and differentiation of large myoid cells containing bundles of striated muscle fibrils. The changes are particularly noteworthy because they first appear during a period in which the animals are known to be developing the capacity to respond immunologically to allografts.
Immunogenetics | 1975
Kenneth H. Roux; E. Peter Volpe
Using the technique of gynogenetic diploidy, which is uniquely suited to amphibians, populations of frog siblings can be obtained in which the allelic diversity at any given gene locus, including histocompatibility loci, is greatly reduced. Analyses of the survival times of skin allografts exchanged among pairs of gynogenetic diploid larvae indicate that allograft rejection is mediated principally by a major histocompatibility complex that codes for strong H-antigens rather than by the cumulative effects of weak antigens controlled by numerous, independently assorting, loci.
Developmental Biology | 1971
Sherill Curtis; E. Peter Volpe
Abstract Extirpation of the thymus, during its differentiation as a lymphoid organ, in the early larval life of the leopard frog was attended by a marked impairment of allograft immunity. In cases in which thymectomy was most successful—i.e., in which no thymic tissue was found in the larvae on later autopsy—the survival of allogeneic grafts was greatly prolonged. When thymectomy was less successful—i.e., when fragments ranging widely in size were found in the larvae at autopsy—the results were variable: the larvae either rejected allografts more slowly than control larvae or responded to them at the same rate as the control larvae. The “less successful” cases of thymectomy most likely represented instances of the regeneration of thymic tissue. The complete removal of the thymus in late larval life, after the thymus had differentiated, was not associated with any discernible decline in immunological capacity. Thus, the debilitating effects on the immune mechanism are demonstrable only when thymectomy is performed during, not after, the development of the thymus. The thymus apparently plays a critical role in the proliferation or maturation of immunologically competent cells during or shortly after its differentiation as a lymphoid organ.
Archive | 1971
Maria Luiza Beçak; Willy Beçak; Franklin L. Roberts; Robert N. Shoffner; E. Peter Volpe; Kurt Benirschke; T. C. Hsu
The pair of large acrocentric autosomes bears a secondary constriction and satellites on the short arm.
Developmental Biology | 1962
E. Peter Volpe; Sanjoy Dasgupta
Abstract A conspicuous variant of the common-spotted leopard frog, Rana pipiens, is the burnsi or nonspotted frog. The expression of the deviant phenotype depends not only on a main mutant gene, B, but also on a complex of minor genes or modifiers, each with a small effect. The mode of mutant action was inferred by studying the phenotypic effects of different doses and combinations of the dominant burnsi gene, B, and its wild-type allele, b. This was accomplished by adding an additional set of chromosomes to the diploid complement, i.e., by producing triploid individuals. Consequently, the numerical change at the main burnsi locus was accompanied by corresponding dosage changes at the modifying loci. Precluding the activity of modifiers, the mutant phenotype is not altered by different doses of the main burnsi gene. The action of the main burnsi gene (B) is so contrary to that of the wild-type allele (b) that its inhibitory effects on spotting prevail even in the presence of an increased dosage of the wild-type allele. Spotting modifiers provide a margin of stability. They are spotting genes in their own right, which serve to mitigate the otherwise strong adverse action of the main burnsi gene. The spotting or “+” modifiers tend to shift the expression of the burnsi phenotype toward a wild-type spotting pattern. However, even increased dosages of the “+” modifiers in a triploid burnsi frog cannot promote the formation of sufficient spots to produce the normal spotting pattern characteristic of the wild type. Other modifiers, nonspotting or “−,” act in the opposite direction; these increase the expressivity of the main burnsi gene. It is postulated that the main burnsi gene (B) is inhibiting completely the production of some substance normally elaborated by its wild-type allele. However, the “+” modifiers ensure the synthesis of a limited amount of the substance to form a few spots in the mutant phenotype, while the “−” modifiers tend to keep the substance below the minimum or threshold level.
Science | 1966
E. Peter Volpe; Bryan M. Gebhardt
Postmetamorphic diploid and triploid frogs that had earlier been joined in parabiotic union from embryonic life until metamorphosis were each found to be chimeric with respect to their blood cells, as revealed in chromosome preparations of cultured leucocytes. Blood cells precursorsmost likely were interchanged when the ex-parabionts shared a common circulation in embryonic life,and the exchanged precursor cells apparently homed in the hematopoietic tissues of the hosts. The tolerance which exparabiotic pairs of frogs exhibit toward grafts of each others skin is attributable to the blood cell chimerism.
Developmental Biology | 1963
E. Peter Volpe
Abstract The semidominant mutant gene burnsi (B) suppresses the formation of the dorsal spots (aggregations of dermal melanophores) that confer upon the wild-type frog (Rana pipiens) its characteristic leopard-like pattern. Mutant action was appraised by analyzing the interaction of contiguous burnsi and wild-type tissues in experimentally produced chimeric frogs. Two embryos in early tailbud development, one burnsi (Bb) and the other wild-type (bb), were each cut in half across the middle of the body, and the genetically different front halves were interchanged. Twenty-four chimeric embryos were carried through and beyond metamorphosis, of which 13 comprised the union of anterior burnsi halves to posterior wild-type halves (burnsi:wild-type) and 11 represented the reverse fusion (wild-type:burnsi). The primary objective was to deduce whether factors endogenous or exogenous to the spot-forming melanophores are primarily responsible for the difference in mutant and wild-type pigmentary patterns. It appears that the mutant burnsi gene alters principally the intrinsic properties of the melanoblasts. That the pigment cell is modified in some way by the mutant gene is suggested by the failure, to a variable extent, of wild-type melanoblasts to form spots in the posterior half of a burnsi:wild-type chimeric frog. A provisional interpretation is that burnsi propigment cells infiltrate the posterior wild-type terrain and inhibit or curtail the aggregative movements of the wild-type melanoblasts. The antagonistic influences of the burnsi melanoblasts may wane as they complete their differentiation. Accordingly, some of the wild-type pigment cells, previously held in abeyance, may then satisfy their inherent tendency to congregate into spots. In the reciprocal chimeric combination, wild-type:burnsi, it is likely that the wild-type melanoblasts invade the burnsi terrain. Once again, impeditive activities of resident burnsi melanoblasts apparently prevent the emigrant wild-type pigment cells from fulfilling their aggregative potential. It may be thought that an accessory inhibiting factor is some unfavorable condition in the tissue environment of the melanoblasts, but data from other lines of inquiry indicate that the burnsi environmental tissue is suitable for the differentiation of wild-type melanoblasts.
Science | 1961
E. Peter Volpe
The genetic distinction between the nonspotted, or burnsi, mutant and the common-spotted, wild-type leopard frog is not simply unifactorial. The burnsi phenotype is a manifestation of genic interaction between a major pigmentary locus and a complex of modifiers (minor genes with small effects).