New record of Andalgalomys olrogi (Rodentia: Sigmodontinae) in Catamarca, Argentina, expands its altitudinal and environmental range

A partir del estudio de dos muestras de egagrópilas de Tyto furcata colectadas en Alumbrera, a 1650m s. n. m. en el extremo norte del Campo del Pucará, departamento Andalgalá, Catamarca, Argentina, presentamos un novedoso registro para el roedor sigmodontino Andalgalomys olrogi Williams & Mares, 1978. Documentamos por primera vez la presencia de esta especie a más de 1300 m de altitud y en un ambiente de pastizales de neblina de Yungas (parcialmente modificados por actividades antrópicas). Su escasa representación en las muestras estudiadas (< 1,6%) sugiere que el Campo del Pucará representa un área marginal dentro de su rango de distribución.We present a novel record for the sigmodontine rodent Andalgalomys olrogi Williams and Mares, 1978, from the analysis of two samples of Tyto furcata pellets collected in Alumbrera, 1650 m a. s. l. at the northern end of Campo del Pucará, Andalgalá department, Catamarca, Argentina. We document the presence of Andalgalomys olrogi at a higher elevation than reported before (more than 1300 m) and in a highland grassland environment of Yungas (partially modified by anthropic activities) for the first time. Its low representation in the studied samples (< 1.6%) suggests that Campo del Pucará represents a marginal area within its range of distributionFil: Günther Ortiz Tempel, P.. Universidad Nacional de Tucumán. Facultad de Ciencias Naturales e Instituto Miguel Lillo; ArgentinaFil: Jayat, Jorge Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - Tucumán. Unidad Ejecutora Lillo; Argentina. Fundación Miguel Lillo; ArgentinaFil: Ortiz, Pablo Edmundo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Instituto Superior de Correlación Geológica. Universidad Nacional de Tucumán. Facultad de Ciencias Naturales e Instituto Miguel Lillo. Departamento de Geología. Cátedra Geología Estructural. Instituto Superior de Correlación Geológica; Argentin

Analyse des remaniements du protéome associés à la levée de dormance d’une graine imbibée

National audienc

Taxonomy based on science is necessary for global conservation

Peer reviewe

A mouse model of pseudohypoaldosteronism type II reveals a novel mechanism of renal tubular acidosis

Pseudohypoaldosteronism type II (PHAII) is a genetic disease characterized by association of hyperkalemia, hyperchloremic metabolic acidosis, hypertension, low renin, and high sensitivity to thiazide diuretics. It is caused by mutations in the WNK1, WNK4, KLHL3 or CUL3 gene. There is strong evidence that excessive sodium chloride reabsorption by the sodium chloride cotransporter NCC in the distal convoluted tubule is involved. WNK4 is expressed not only in distal convoluted tubule cells but also in β-intercalated cells of the cortical collecting duct. These latter cells exchange intracellular bicarbonate for external chloride through pendrin, and therefore, account for renal base excretion. However, these cells can also mediate thiazide-sensitive sodium chloride absorption when the pendrin-dependent apical chloride influx is coupled to apical sodium influx by the sodium-driven chloride/bicarbonate exchanger. Here we determine whether this system is involved in the pathogenesis of PHAII. Renal pendrin activity was markedly increased in a mouse model carrying a WNK4 missense mutation (Q562E) previously identified in patients with PHAII. The upregulation of pendrin led to an increase in thiazide-sensitive sodium chloride absorption by the cortical collecting duct, and it caused metabolic acidosis. The function of apical potassium channels was altered in this model, and hyperkalemia was fully corrected by pendrin genetic ablation. Thus, we demonstrate an important contribution of pendrin in renal regulation of sodium chloride, potassium and acid-base homeostasis and in the pathophysiology of PHAII. Furthermore, we identify renal distal bicarbonate secretion as a novel mechanism of renal tubular acidosis.Pseudohypoaldosteronism type II (PHAII) is a genetic disease characterized by association of hyperkalemia, hyperchloremic metabolic acidosis, hypertension, low renin, and high sensitivity to thiazide diuretics. It is caused by mutations in the WNK1, WNK4, KLHL3 or CUL3 gene. There is strong evidence that excessive sodium chloride reabsorption by the sodium chloride cotransporter NCC in the distal convoluted tubule is involved. WNK4 is expressed not only in distal convoluted tubule cells but also in beta-intercalated cells of the cortical collecting duct. These latter cells exchange intracellular bicarbonate for external chloride through pendrin, and therefore, account for renal base excretion. However, these cells can also mediate thiazide-sensitive sodium chloride absorption when the pendrin-dependent apical chloride influx is coupled to apical sodium influx by the sodium-driven chloride/bicarbonate exchanger. Here we determine whether this system is involved in the pathogenesis of PHAII. Renal pendrin activity was markedly increased in a mouse model carrying a WNK4 missense mutation (Q562E) previously identified in patients with PHAII. The upregulation of pendrin led to an increase in thiazide-sensitive sodium chloride absorption by the cortical collecting duct, and it caused metabolic acidosis. The function of apical potassium channels was altered in this model, and hyperkalemia was fully corrected by pendrin genetic ablation. Thus, we demonstrate an important contribution of pendrin in renal regulation of sodium chloride, potassium and acid-base homeostasis and in the pathophysiology of PHAII. Furthermore, we identify renal distal bicarbonate secretion as a novel mechanism of renal tubular acidosis