Ecology: is speciation driven by species diversity?

Emerson and Kolm show that the proportion of species endemic to an island is positively related to its species richness and, assuming that endemism indexes speciation rate, they infer that greater species diversity accelerates diversification. Here we demonstrate that the same correlation between species richness and percentage endemism can arise even if within-island speciation is negligible, particularly when both endemism and species richness depend on attributes of islands (such as area) that influence the average age of resident populations. Island biogeography theory indicates that, where the average time to extinction is relatively long, diversity increases through colonization, irrespective of whether new species are formed; at the same time, islands on which populations persist for longer accumulate more endemic species as local populations differentiate and populations on neighbouring islands become extinct. We therefore suggest that species richness and endemism are correlated fortuitously owing to their mutual dependence on the life spans of populations on islands, which is unrelated to speciation itself.     

Cholinesterases are down-expressed in human colorectal carcinoma

The aberrations of cholinesterase (ChE) genes and the variation of ChE activity in cancerous tissues prompted us to investigate the expression of ChEs in colorectal carcinoma. The study of 55 paired specimens of healthy (HG) and cancerous gut (CG) showed that acetylcholinesterase (AChE) activity fell by 32% and butyrylcholinesterase (BuChE) activity by 58% in CG. Abundant AChE-H, fewer AChE-T, and even fewer AChE-R and BuChE mRNAs were observed in HG, and their content was greatly diminished in CG. The high level of the AChE-H mRNA explains the abundance of AChE-H subunits in HG, which as glycosylphosphatidylinositol (GPI)-anchored amphiphilic AChE dimers (G₂^A) and monomers (G₁^A) account for 69% of AChE activity. The identification of AChE-T and BuChE mRNAs justifies the occurrence in gut of A₁₂, G₄^H and PRiMA-containing G₄^A AChE forms, besides G₄^H, G₄^A and G₁^H BuChE. The down-regulation of ChEs might contribute to gut carcinogenesis by increasing acetylcholine availability and overstimulating muscarinic receptors. Received 19 May 2006; received after revision 5 June 2006; accepted 5 July 2006