Biomedical subjects

L A Caron

Publications and source records attributed to L A Caron.

4 recordsLinked to original sources

PubMed1997

Resistance, susceptibility, and immunity to Eimeria tenella in major histocompatibility (B) complex congenic lines.

The major histocompatibility (B) complex influence on resistance, susceptibility, and immunity to Eimeria tenella was examined in UCD B complex congenic chicken lines. In Experiment 1, 6-wk-old chicks from 12 UCD congenic lines were weighed and assigned to either challenge or control groups. The challenge group received a dose of 10,000 E. tenella oocysts. Response to challenge was evaluated by body weight gain and cecal lesion scores. Cecal lesion scores in B3B3 chickens were significantly lower than those of all other genotypes. Genotype B2B2 had the highest lesion scores, which were significantly different from the lesion scores calculated for B3B3, B18B18, and B21B21 chickens but were not significantly different from B14B14, B15B15, B17B17, B19B19, B24B24, BCBC, BJBJ, and BQBQ genotypes. The B21B21 chickens had significantly lower lesion scores than B2B2, B14B14, and BCBC chickens. No other significant lesion score differences were found among the remaining lines. The highest weight gain found in B19B19 chickens was significantly different from that of B3B3, B14B14, B15B15, B17B17, B18B18, B24B24, and BCBC chickens. The B15B15 chickens had the lowest weight gain, which was significantly different from that of B2B2, B19B19, B21B21, B24B24, BJBJ, and BQBQ chickens. Experiment 2 tested the immune response to E. tenella after low dose oocyst immunization. Chicks from 10 UCD 003 congenic lines were divided into three groups: control, challenge, and immune. At 5 wk of age, the immune group was immunized with 500 E. tenella oocysts for 5 consecutive d. Fourteen days after the last immunization all chicks were weighed, and 10,000 E. tenella oocysts were administered to the challenge and immune groups. Significant lesion score differences existed among all three treatments: control (0), immune (2.14 +/- 0.1); challenge (3.13 +/- 0.1). Among immune birds, B3B3 and BQBQ chickens had significantly lower lesion scores than B19B19, B24B24, B14B14, and B2B2 chickens. Neither B19B19 nor B24B24 chickens were well-protected, as indicated by their higher lesion scores. No significant differences in weight gain were found in immune birds. The B complex affected resistance and susceptibility as well as the immune response to E. tenella. Cecal lesion scores following challenge in naive birds or after immunization were influenced by the B complex, whereas weight gain was affected in naive birds only. These effects may be manifested through differences in immune competence at the time of challenge or immunization, the amount of parasite antigen production, or the threshold doses for effective immunization.

Analysis of Variance↗

PubMed1993

An activated Notch receptor blocks cell-fate commitment in the developing Drosophila eye.

The Notch locus of Drosophila melanogaster encodes a 2,703-amino-acid transmembrane protein required for a variety of developmental processes, including neurogenesis, oogenesis and ommatidial assembly. The Notch protein contains a large extracellular domain of 36 epidermal growth factor-like repeats as well as three Notch/Lin-12 repeats and an intracellular domain with 6 Cdc10/ankyrin repeats, motifs that are highly conserved in several vertebrate Notch homologues. Truncation of the extracellular domain of the Drosophila Notch protein produces an activated receptor, as judged by its ability to cause phenotypes similar to gain-of-function alleles of duplications of the Notch locus. Equivalent truncations of vertebrate Notch-related proteins have been associated with malignant neoplasma and other developmental abnormalities. We present here an analysis of activated Notch function at single-cell resolution in the Drosophila compound eye. We find that overexpression of full-length Notch in defined cell types has no apparent effects but that overexpression of activated Notch in the same cells transiently blocks their proper cell-fate commitment, causing them either to adopt incorrect cell fates or to differentiate incompletely. Moreover, an activated Notch protein lacking the transmembrane domain is translocated to the nucleus, raising the possibility that Notch may participate directly in nuclear events.

Animals↗

PubMed1992

The involvement of the Notch locus in Drosophila oogenesis.

The Notch gene in Drosophila encodes a transmembrane protein with homology to EGF that, in a variety of tissues, appears to mediate cell interactions necessary for cell fate choices. Here we demonstrate that oogenesis and spermatogenesis depend on Notch. We examine the phenotypes of the temperature-sensitive Notch allele, Nts1, and, using a monoclonal antibody, determine the cellular and subcellular distribution of Notch protein during oogenesis. We show that Nts1 is associated with a missense mutation in the extracellular, EGF homologous region of Notch and that at non-permissive temperatures oogenesis is blocked and the subcellular distribution of the protein is altered. In wild-type ovaries, Notch protein is found on the apical surface of somatically derived follicle cells, while in the germline-derived cells the protein is not polarized. These findings are discussed in view of the hypothesis that Notch acts as a multifunctional receptor to mediate developmentally important cell interactions.

Animals↗

PubMed1987

Glucocorticoid action on the immune system.

Glucocorticoids have profound effects on immune function that are mediated, in part, by steroid-induced cell death. Our studies have been aimed at identifying the mechanism of this lymphocytolytic process using the rat thymocyte as a model system. Administration of glucocorticoids in vivo resulted in internucleosomal cleavage of the lymphocyte genome that was detectable within 2 h of treatment and increased with time after hormone administration. Six h after steroid treatment greater than 50% of the genome was degraded, yet cell viability remained greater than 90% indicating that this event preceded cell death. Furthermore, this process appeared to be mediated by the glucocorticoid receptor since the antagonist RU 486 blocked glucocorticoid-mediated DNA degradation. To further characterize this lymphocytolysis we have analyzed glucocorticoid-treated thymocytes for nucleases. Two families of nuclear proteins have been identified, a 30-32 kDa doublet and a series of 3-4 proteins that are 12-19 kDa, both of which are induced by glucocorticoid treatment (137 +/- 6% and 342 +/- 24%, respectively) and have prominent nuclease activity. These nucleases can also be induced in vitro indicating that glucocorticoids act directly on thymocytes to mediate this response. Moreover, this nuclease induction, like glucocorticoid-mediated DNA degradation, could be blocked by RU 486. Based on these findings we propose a working model of glucocorticoid-mediated lymphocytolysis in which these steroids, acting via a receptor mediated process, induce the expression of a lysis gene product (nuclease) which degrades the genome and results in cell death.

Animals↗