Performance of wild animals with "broken" traits: Movement patterns in nature of moose with leg injuries.

Organismal traits are presumed to be well suited for performance in the tasks required for survival, growth, and reproduction. Major injuries to such traits should therefore compromise performance and prevent success in the natural world; yet some injured animals can survive for long periods of time and contribute to future generations. We here examine 3 years of camera trap observations along a remote trail through old-growth forest in northern British Columbia, Canada. The most common observations were of moose (2966), wolves (476), and brown bears (224). The moose overwhelmingly moved in one direction along the trail in the late fall and early winter and in the other direction in the spring. This movement was clustered/contagious, with days on which many moose traveled often being interspersed with days on which few moose traveled. On the video recordings, we identified 12 injured moose, representing 1.4% of all moose observations. Seven injuries were to the carpus, three were to the antebrachium, and two were to the tarsus-and they are hypothesized to reflect damage to ligaments, tendons, and perhaps bones. The injured moose were limping in all cases, sometimes severely; and yet they did not differ noticeably from uninjured moose in the direction, date, contagiousness, or speed of movement along the trail. We discuss the potential relevance of these findings for the action of natural selection in the evolution of organismal traits important for performance.

Parietal foramina with cleidocranial dysplasia is caused by mutation in MSX2.

The combination of skull defects in the form of enlarged parietal foramina (PFM) and deficient ossification of the clavicles is known as parietal foramina with cleidocranial dysplasia (PFMCCD). It is considered to be distinct from classical cleidocranial dysplasia (CCD) and is listed as a separate OMIM entry (168550). So far, only two families have been reported and the molecular basis of the disorder is unknown. We present a third family with PFMCCD, comprising four affected individuals in three generations, and demonstrate that a heterozygous tetranucleotide duplication in the MSX2 homeobox gene (505_508dupATTG) segregates with the phenotype. PFMCCD is indeed aetiologically distinct from CCD, which is caused by mutations in the RUNX2 gene, but allelic with isolated PFM, in which MSX2 mutations were previously identified. Our observations highlight the role of MSX2 in clavicular development and the importance of radiological examination of the clavicles in subjects with PFM.