Life cycle of Trichostrongylus retortaeformis in its natural host,the rabbit (Oryctolagus cuniculus)

The chronology of the life cycle of Trichostrongylus retortaeformis (Zeder, 1800) (Nematoda, Trichostrongyloidea) is studied in its natural host Oryctolagus cuniculus. The free living period lasted 5 days at 24 degrees C. Worm-free rabbits were each infected per os with T. retortaeformis larvae. Rabbits were killed at 12 h post-infection (p.i.) and every day from one day to 13 days p.i. By 12 h p.i., all the larvae were exsheathed and in the small intestine. The third moult occurred between 3 and 5 days p.i. and the last moult between 4 and 7 days p.i. The prepatent period lasted 12 to 13 days. The patent period lasted five and a half months. The four known life cycles of species of Trichostrongylus in ruminants were compared with that of T. retortaeformis. No significant difference was found except in the duration of the prepatent period. These similarities in the life cycles confirm the previously formulated hypotheses on the relationship between the parasites of the two host groups (Durette-Desset, 1985).     

Lack of intraspecific variation in the second Internal Transcribed Spacer (ITS-2) of Trichostrongylus colubriformis ribosomal DNA

The nucleotide sequence of the second internal transcribed spacer (ITS-2) was determined for three populations of the parasitic nematode Trichostrongylus colubriformis which differed in their susceptibility to benzimidazole anthelmintics and/or in their geographical origin. No intraspecific variation was found in the ITS-2 sequence, indicating that this region of rDNA is inadequate to discriminate between resistant and susceptible populations of T. colubriformis, but it may prove useful for distinguishing between species of Trichostrongylus.     

The endocrine control of phase transition: some new aspects

Abstract. The present article summarizes some recent findings relating to the underlying mechanism of phase transition in locusts, from the nonswarming solitarious phase to the swarming gregarious phase. These phases differ in many traits, such as colouration, morphometrics and behaviour. The most comprehensive theory at present to explain the switch from the nonswarming to the swarming form is that the locusts are brought together by the heterogeneity of the environment. They gather at preferential structures and food plants and physical contact then stimulates individuals to gregarize. Phase change can also be transferred across generations by maternal pheromones. The endocrine regulation of phase polymorphism is still not fully understood. The role of ecdysteroids has been studied, so far with no final conclusion. It is remarkable that the prothoracic glands persist longer in isolated-reared adults, which implies that these glands continue to play a role, although they no longer release important amounts of ecdysteroids. Juvenile Hormone, without any doubt, induces certain solitarious characteristics, such as green colouration, but is not the primary causal factor. A real breakthrough was the discovery of [His⁷]-corazonin, made possible by using a novel assay system, the Okinawa albino mutant of Locusta migratoria , which was known to be deficient in this hormone. This peptide, which is produced in the brain and is most likely released via the corpora cardiaca, promotes the gregarious black pigmentation. It also plays a role in morphometrical phase change as well as in behavioural alterations. Corazonin is apparently quite an important peptide not only in locusts, but also in insects in general.     

The yeast APC/C subunit Mnd2 prevents premature sister chromatid separation triggered by the meiosis-specific APC/C-Ama1

Cohesion established between sister chromatids during pre-meiotic DNA replication mediates two rounds of chromosome segregation. The first division is preceded by an extended prophase wherein homologous chromosomes undergo recombination. The persistence of cohesion during prophase is essential for recombination and both meiotic divisions. Here we show that Mnd2, a subunit of the anaphase-promoting complex (APC/C) from budding yeast, is essential to prevent premature destruction of cohesion in meiosis. During S- and prophase, Mnd2 prevents activation of the APC/C by a meiosis-specific activator called Ama1. In cells lacking Mnd2 the APC/C-Ama1 enzyme triggers degradation of Pds1, which causes premature sister chromatid separation due to unrestrained separase activity. In vitro, Mnd2 inhibits ubiquitination of Pds1 by APC/C-Ama1 but not by other APC/C holo-enzymes. We conclude that chromosome segregation in meiosis depends on the selective inhibition of a meiosis-specific form of the APC/C.     

Epidermal Cadm1 expression promotes autoimmune alopecia via enhanced T cell adhesion and cytotoxicity

Autoimmune alopecia is characterized by an extensive epidermal T cell infiltrate that mediates hair follicle destruction. We have investigated the role of cell adhesion molecule 1 (Cadm1; Necl2) in this disease. Cadm1 is expressed by epidermal cells and mediates heterotypic adhesion to lymphocytes expressing class 1-restricted T cell-associated molecule (CRTAM). Using a murine autoimmune alopecia model, we observed an increase in early-activated cytotoxic (CD8-restricted, CRTAM-expressing) T cells, which preferentially associated with hair follicle keratinocytes expressing Cadm1. Coculture with Cadm1-transduced MHC-matched APCs stimulated alopecic lymph node cells to release IL-2 and IFN-γ. Overexpression of Cadm1 in cultured human keratinocytes did not promote cytokine secretion, but led to increased adhesion of alopecic cytotoxic T cells and enhanced T cell cytotoxicity in an MHC-independent manner. Epidermal overexpression of Cadm1 in transgenic mice led to increased autoimmune alopecia susceptibility relative to nontransgenic littermate controls. Our findings reveal that Cadm1 expression in the hair follicle plays a role in autoimmune alopecia.