Effects of convict cichlids on growth and recruitment of White River springfish

Observations of changes in population density of native White River springfish ( Crenichthys baileyi ) in Pahranagat Valley led to the following hypothesis: introduced convict cichlids ( Cichlasoma nigrofasciatum ) cause reduced growth and recruitment; cover reduces the magnitude of the effect. The hypothesis was tested by establishing sympatric and allopatric groups of the two species in experimental aquaria with and without cover. Change in volume (= mass) and length of the two species over a three-month period in spring 1986 and 1987 was measured and analyzed using 2 × 2 factorial analyses. Convict cichlids caused reduced growth and eliminated recruitment of springfish under the experimental conditions. Cover did not influence growth but positively affected recruitment of springfish in allopatry. It is likely that a portion of the reduced springfish population densities in nature can be attributed to adverse effects from introduced cichlids.     

Dampening of death pathways by schnurri-2 is essential for T-cell development

Generation of a diverse and self-tolerant T-cell repertoire requires appropriate interpretation of T-cell antigen receptor (TCR) signals by CD4(+?) CD8(+) double-positive thymocytes. Thymocyte cell fate is dictated by the nature of TCR-major-histocompatibility-complex (MHC)-peptide interactions, with signals of higher strength leading to death (negative selection) and signals of intermediate strength leading to differentiation (positive selection). Molecules that regulate T-cell development by modulating TCR signal strength have been described but components that specifically define the boundaries between positive and negative selection remain unknown. Here we show in mice that repression of TCR-induced death pathways is critical for proper interpretation of positive selecting signals in vivo, and identify schnurri-2 (Shn2; also known as Hivep2) as a crucial death dampener. Our results indicate that Shn2(-/-) double-positive thymocytes inappropriately undergo negative selection in response to positive selecting signals, thus leading to disrupted T-cell development. Shn2(-/-) double-positive thymocytes are more sensitive to TCR-induced death in vitro and die in response to positive selection interactions in vivo. However, Shn2-deficient thymocytes can be positively selected when TCR-induced death is genetically ablated. Shn2 levels increase after TCR stimulation, indicating that integration of multiple TCR-MHC-peptide interactions may fine-tune the death threshold. Mechanistically, Shn2 functions downstream of TCR proximal signalling compenents to dampen Bax activation and the mitochondrial death pathway. Our findings uncover a critical regulator of T-cell development that controls the balance between death and differentiation.     

Bats of the Colorado oil shale region

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