Behavioral activities and breeding success of Willow Flycatchers in the Sierra Nevada

Observing survival and how individuals allocate time can provide insight into a species' ability to tolerate environmental constraints. We studied the Willow Flycatcher ( Empidonax trallii ) in the Sierra Nevada to determine if there were behavioral differences between pairs that successfully produced offspring and those that did not. This information will advance understanding of why these birds are declining in the Sierra Nevada and contribute to recommendations that may help to conserve them. We studied birds in 13 meadows in 2000 and 2001 using continuous focal-animal observations. Of the 43 territories we observed, 11 were occupied by males who never paired with a female, leaving 32 pairs for analysis. Of the 32 pairs, 13 were successful at breeding on their 1st attempt, and 9 pairs failed at their initial try but were successful on their 2nd breeding attempt. Throughout the breeding season, Willow Flycatchers spent 77%-78% of the day loafing during territory establishment and nest building, and loafing reached a low of 49% of the time budget during the nestling stage. Unsuccessful pairs spent on average 34% more time perching than their successful counterparts, while successful pairs spent on average 48% more of their time on the nest than unsuccessful pairs. Willow Flycatchers doubled the time spent foraging during the nestling phase because they had to meet the daily intake requirements for their young and themselves. Our results suggest that birds that spent more time on the nest and less time vocalizing had a significantly higher probability of successfully producing young because they were able to protect nests from predators, nest parasites, and inclement weather.     

KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron

Familial hyperkalemic hypertension (FHHt) is a Mendelian form of arterial hypertension that is partially explained by mutations in WNK1 and WNK4 that lead to increased activity of the Na(+)-Cl(-) cotransporter (NCC) in the distal nephron. Using combined linkage analysis and whole-exome sequencing in two families, we identified KLHL3 as a third gene responsible for FHHt. Direct sequencing of 43 other affected individuals revealed 11 additional missense mutations that were associated with heterogeneous phenotypes and diverse modes of inheritance. Polymorphisms at KLHL3 were not associated with blood pressure. The KLHL3 protein belongs to the BTB-BACK-kelch family of actin-binding proteins that recruit substrates for Cullin3-based ubiquitin ligase complexes. KLHL3 is coexpressed with NCC and downregulates NCC expression at the cell surface. Our study establishes a role for KLHL3 as a new member of the complex signaling pathway regulating ion homeostasis in the distal nephron and indirectly blood pressure.