Producer-decomposer co-dependency influences biodiversity effects

Producers, such as plants and algae, acquire nutrients from inorganic sources that are supplied primarily by decomposers whereas decomposers, mostly fungi and bacteria, acquire carbon from organic sources that are supplied primarily by producers. This producer-decomposer co-dependency is important in governing ecosystem processes, which implies that the impacts of declining biodiversity on ecosystem functioning should be strongly influenced by this process. Here we show, by simultaneously manipulating producer (green algal) and decomposer (heterotrophic bacterial) diversity in freshwater microcosms, that algal biomass production varies considerably among microcosms (0.0-0.67 mg ml(-1)), but that neither algal nor bacterial diversity by itself can explain this variation. Instead, production is a joint function of both algal and bacterial diversity. Furthermore, the range in algal production in microscosms in which bacterial diversity was manipulated was nearly double (1.82 times) that of microcosms in which bacterial diversity was not manipulated. Measures of organic carbon use by bacteria in these microcosms indicate that carbon usage is the mechanism responsible for these results. Because both producer and microbial diversity respond to disturbance and habitat modification, the main causes of biodiversity loss, these results suggest that ecosystem response to changing biodiversity is likely to be more complex than other studies have shown.     

Mutations in ABCC6 cause pseudoxanthoma elasticum

Pseudoxanthoma elasticum (PXE) is a heritable disorder of the connective tissue. PXE patients frequently experience visual field loss and skin lesions, and occasionally cardiovascular complications. Histopathological findings reveal calcification of the elastic fibres and abnormalities of the collagen fibrils. Most PXE patients are sporadic, but autosomal recessive and dominant inheritance are also observed. We previously localized the PXE gene to chromosome 16p13.1 (refs 8,9) and constructed a physical map. Here we describe homozygosity mapping in five PXE families and the detection of deletions or mutations in ABCC6 (formerly MRP6) associated with all genetic forms of PXE in seven patients or families.