No abstract

Allen's Rule documents a century-old biological observation that strong positive correlations exist among latitude, ambient temperature, and limb length in mammals. Although genetic selection for thermoregulatory adaptation is frequently presumed to be the primary basis of this phenomenon, important but frequently overlooked research has shown that appendage outgrowth is also markedly influenced by environmental temperature. Alteration of limb blood flow via vasoconstriction/vasodilation is the current default hypothesis for this growth plasticity, but here we show that tissue perfusion does not fully account for differences in extremity elongation in mice. We show that peripheral tissue temperature closely reflects housing temperature in vivo, and we demonstrate that chondrocyte proliferation and extracellular matrix volume strongly correlate with tissue temperature in metatarsals cultured without vasculature in vitro. Taken together, these data suggest that vasomotor changes likely modulate extremity growth indirectly, via their effects on appendage temperature, rather than vascular nutrient delivery. When combined with classic evolutionary theory, especially genetic assimilation, these results provide a potentially comprehensive explanation of Allen's Rule, and may substantially impact our understanding of phenotypic variation in living and extinct mammals, including humans.Allen's Rule ͉ bone growth ͉ bone tissue culture ͉ cartilage biology ͉ thermoregulation E cogeographical rules relating climate to extremity length and body mass have long been central tenets of biology, and are among the best supported observations in natural-dwelling species (1). Allen's Rule codifies the observation that appendages (ears, limbs, and tails) of animals living in cold geographical regions are consistently shorter than those of closely related counterparts occupying warmer climes (2). Shortened extremities minimize heat loss by reducing surface area relative to volume and have long been viewed as genetically determined thermoregulatory adaptations (1). However, the heritability of extremity length is largely unknown, because similar phenotypes can be reproduced in laboratory mammals by modifying their ambient rearing temperature (3-6) (Fig. 1). The mechanism by which environmental temperature modulates extremity growth has remained elusive (7,8). Understanding growth plasticity is critical to basic evolutionary analyses, because many characters that have long been hypothesized to be adaptations may instead be partial or even entirely effects of ambient temperature (9, 10). Moreover, knowledge of this phenotypic plasticity will be a key factor in ecological conservation strategies for anticipated changes in global climate that may have direct impacts on human economics and sustainability (11).The traditional explanation for temperature-growth effects in skeletal extremities is an altered supply of essential nutrients and growth factors via increased or decreased blood flow that results from changes in vasomotor tone (i.e., t...

Degenerate oligonucleotide primers were synthesized to amplify nucleotide sequences from portions of the fusion protein and matrix protein genes of Newcastle disease virus (NDV) genomic RNA that could be used diagnostically. These primers were used in a single-tube reverse transcription PCR of NDV genomic RNA coupled to direct nucleotide sequencing of the amplified product to characterize more than 30 NDV isolates. In agreement with previous reports, differences in the fusion protein cleavage sequence that correlated genotypically with virulence among various NDV pathotypes were detected. By using sequences generated from the matrix protein gene coding for the nuclear localization signal, lentogenic viruses were again grouped phylogenetically separate from other pathotypes. These techniques were applied to compare neurotropic velogenic viruses isolated from an outbreak of Newcastle disease in cormorants and turkeys. Cormorant NDV isolates and an NDV isolate from an infected turkey flock in North Dakota had the fusion protein cleavage sequence 109 SRGRRQKRFVG 119. The R-for-G substitution at position 110 may be unique for the cormoranttype isolates. Although the amino acid sequences from the fusion protein cleavage site were identical, nucleotide sequence data correlate the outbreak in turkeys to a cormorant virus isolate from Minnesota and not to a cormorant virus isolate from Michigan. On the basis of sequence information, the cormorant isolates are virulent viruses related to isolates of psittacine origin, possibly genotypically distinct from other velogenic NDV isolates. These techniques can be used reliably for Newcastle disease epidemiology and for prediction of pathotypes of NDV isolates without traditional live-bird inoculations.