Coyote-badger associations

Four observations made in Jackson Hole, Wyoming, indicate that coyote–badger associations are best considered as phoretic (accidental and nonobligatory) rather than a form of social symbiosis as has been previously suggested.     

Vegetal responses and big game values after thinning regenerating lodgepole pine

Understory vegetal response was found to significantly increase with the degree of thinning in an early regenerating, dense stand of lodgepole pine ( Pinus contorta ). The value of the increased vegetation for deer and elk was determined to be important through comparisons with known dietary and habitat preferences.     

Vegetal change on a northern Utah foothill range in the absence of livestock grazing between 1948 and 1982

Reexamination of a semiarid foothill rangeland, first evaluated in 1948, indicated that secondary succession continues to shift toward a perennial grass-forb community formerly dominated by xeric shrubs, particularly big sagebrush ( Artemisia tridentata spp. vaseyana ). The direct role in livestock grazing in establishment and maintenance of shrub-dominant plant communities appears confirmed in the decline of shrubs upon cessation of livestock grazing in summer and continued browsing by mule deer in winter. The reduction of shrub forages on mule deer winter ranges is a major factor in population declines.     

Inactivation of the proximal NPXY motif impairs early steps in LRP1 biosynthesis

The proximal NPXY and distal NPXYXXL motifs in the intracellular domain of LRP1 play an important role in regulation of the function of the receptor. The impact of single and double inactivating knock-in mutations of these motifs on receptor maturation, cell surface expression, and ligand internalization was analyzed in mutant and control wild-type mice and MEFs. Single inactivation of the proximal NPXY or in combination with inactivation of the distal NPXYXXL motif are both shown to be associated with an impaired maturation and premature proteasomal degradation of full-length LRP1. Therefore, only a small mature LRP1 pool is able to reach the cell surface resulting indirectly in severe impairment of ligand internalization. Single inactivation of the NPXYXXL motif revealed normal maturation, but direct impairment of ligand internalization. In conclusion, the proximal NPXY motif proves to be essential for early steps in the LRP1 biosynthesis, whereas NPXYXXL appears rather relevant for internalization.     

Mutations in the gene encoding GlyT2 (SLC6A5) define a presynaptic component of human startle disease

Hyperekplexia is a human neurological disorder characterized by an excessive startle response and is typically caused by missense and nonsense mutations in the gene encoding the inhibitory glycine receptor (GlyR) alpha1 subunit (GLRA1). Genetic heterogeneity has been confirmed in rare sporadic cases, with mutations affecting other postsynaptic glycinergic proteins including the GlyR beta subunit (GLRB), gephyrin (GPHN) and RhoGEF collybistin (ARHGEF9). However, many individuals diagnosed with sporadic hyperekplexia do not carry mutations in these genes. Here we show that missense, nonsense and frameshift mutations in SLC6A5 (ref. 8), encoding the presynaptic glycine transporter 2 (GlyT2), also cause hyperekplexia. Individuals with mutations in SLC6A5 present with hypertonia, an exaggerated startle response to tactile or acoustic stimuli, and life-threatening neonatal apnea episodes. SLC6A5 mutations result in defective subcellular GlyT2 localization, decreased glycine uptake or both, with selected mutations affecting predicted glycine and Na+ binding sites.     

IFT80, which encodes a conserved intraflagellar transport protein, is mutated in Jeune asphyxiating thoracic dystrophy

Jeune asphyxiating thoracic dystrophy, an autosomal recessive chondrodysplasia, often leads to death in infancy because of a severely constricted thoracic cage and respiratory insufficiency; retinal degeneration, cystic renal disease and polydactyly may be complicating features. We show that IFT80 mutations underlie a subset of Jeune asphyxiating thoracic dystrophy cases, establishing the first association of a defective intraflagellar transport (IFT) protein with human disease. Knockdown of ift80 in zebrafish resulted in cystic kidneys, and knockdown in Tetrahymena thermophila produced shortened or absent cilia.