Disruptive coloration and background pattern matching

Effective camouflage renders a target indistinguishable from irrelevant background objects. Two interrelated but logically distinct mechanisms for this are background pattern matching (crypsis) and disruptive coloration: in the former, the animal's colours are a random sample of the background; in the latter, bold contrasting colours on the animal's periphery break up its outline. The latter has long been proposed as an explanation for some apparently conspicuous coloration in animals, and is standard textbook material. Surprisingly, only one quantitative test of the theory exists, and one experimental test of its effectiveness against non-human predators. Here we test two key predictions: that patterns on the body's outline should be particularly effective in promoting concealment and that highly contrasting colours should enhance this disruptive effect. Artificial moth-like targets were exposed to bird predation in the field, with the experimental colour patterns on the 'wings' and a dead mealworm as the edible 'body'. Survival analysis supported the predictions, indicating that disruptive coloration is an effective means of camouflage, above and beyond background pattern matching.     

Deletion of active ADAMTS5 prevents cartilage degradation in a murine model of osteoarthritis

Human osteoarthritis is a progressive disease of the joints characterized by degradation of articular cartilage. Although disease initiation may be multifactorial, the cartilage destruction appears to be a result of uncontrolled proteolytic extracellular matrix destruction. A major component of the cartilage extracellular matrix is aggrecan, a proteoglycan that imparts compressive resistance to the tissue. Aggrecan is cleaved at a specific 'aggrecanase' site in human osteoarthritic cartilage; this cleavage can be performed by several members of ADAMTS family of metalloproteases. The relative contribution of individual ADAMTS proteases to cartilage destruction during osteoarthritis has not been resolved. Here we describe experiments with a genetically modified mouse in which the catalytic domain of ADAMTS5 (aggrecanase-2) was deleted. After surgically induced joint instability, there was significant reduction in the severity of cartilage destruction in the ADAMTS5 knockout mice compared with wild-type mice. This is the first report of a single gene deletion capable of abrogating the course of cartilage destruction in an animal model of osteoarthritis. These results demonstrate that ADAMTS5 is the primary 'aggrecanase' responsible for aggrecan degradation in a murine model of osteoarthritis, and suggest rational strategies for therapeutic intervention in osteoarthritis.     

Activation of complement by trypanosomes

Summary Factors exhibiting anti-complementary activity released from trypanosomes after incubation at 20°C were described. The active material was shown to consume the first component of bovine complement. While the anticomplementary factor(s) from T. lewisi could activate bovine, human and guinea pig complement, the factor(s) from T. congolense was observed to activate bovine complement, but not guinea pig and only slightly human complement. The roles of complement activating factor(s) of trypanosomes in the pathology of the disease are discussed.This project is supported by National Research Council of Canada grant A 0068 and a grant from the International Development Research Centre.     

Predicted recurrences of mass coral mortality in the Indian Ocean

In 1998, more than 90% of shallow corals were killed on most Indian Ocean reefs. High sea surface temperature (SST) was a primary cause, acting directly or by interacting with other factors. Mean SSTs have been forecast to rise above the 1998 values in a few decades; however, forecast SSTs rarely flow seamlessly from historical data, or may show erroneous seasonal oscillations, precluding an accurate prediction of when lethal SSTs will recur. Differential acclimation by corals in different places complicates this further. Here I scale forecast SSTs at 33 Indian Ocean sites where most shallow corals died in 1998 (ref. 1) to identify geographical patterns in the timing of probable repeat occurrences. Reefs located 10-15 degrees south will be affected every 5 years by 2010-2025. North and south from this, dates recede in a pattern not directly related to present SSTs; paradoxically, some of the warmest sites may be affected last. Temperatures lethal to corals vary in this region by 6 degrees C, and acclimation of a modest 2 degrees C by corals could prolong their survival by nearly 100 years.