Jan B DeJarnette

Recent studies on invasive species have led to the development of an apparent paradox when trying to explain how populations succeed after experiencing genetic bottlenecks in their new environments. Many introduced populations retain genetic diversity from multiple introduction events, but others that resulted from a single introduction event are expected to have low genetic diversity and low evolutionary potential. Introduced Black Spiny-Tailed Iguanas (Ctenosaura similis) on a barrier island (Keewaydin Island [KI]) in subtropical Florida are thought to be the result of a single introduction of a small founder group, although this population has expanded significantly since its founding in 1995. We investigated the presence of this genetic paradox by determining the genetic variation of this introduced population. We extracted DNA from muscle tissue samples (N = 21) and sequenced a region of the ND4 gene to allow for comparison with previously described native Ctenosaura populations. We documented a single haplotype from KI, which means this iguana population likely descended from a single introduction event and one geographic source population (Honduras). If this single haplotype represents an overall reduction in genetic diversity, then this population demonstrates that genetic variability is not always necessary for a species to become established in a new ecological range. This interpretation may have strong implications for invasive species management.

The T cell antigen receptor (TCR) and pre-TCR complexes are composed of multiple signal-transducing subunits (CD3γ, CD3δ, CD3ε, and ζ) that each contain one or more copies of a semiconserved functional motif, the immunoreceptor tyrosine-based activation motif (ITAM). Although biochemical studies indicate that individual TCR-ITAMs may bind selectively or with different affinity to various effector molecules, data from other experiments suggest that at least some ITAMs are functionally equivalent. In this study, we examined the role of CD3ε ITAM-mediated signals in T cell development by genetically reconstituting CD3ε-deficient mice with transgenes encoding either wild-type or ITAM-mutant (signaling defective) forms of the protein. The results demonstrate that signals transduced by CD3ε are not specifically required for T cell maturation but instead contribute quantitatively to TCR signaling in a manner similar to that previously observed for ζ chain. Unexpectedly, analysis of TCR-transgenic/CD3ε-mutant mice reveals a potential role for CD3ε signals in T cell survival.