Seasonal variation in fish trophic networks in two clear-water streams in the Central Llanos region, Venezuela

Food webs are not static entities; consumer resource interactions vary in both time and space, which complicates depiction and comparisons of food web structures. We estimated fish assemblage structure and diets in two clear-water streams in the Venezuelan Llanos region (Charcote and Charcotico) and constructed trophic networks (sub-webs defined by fishes as the principal consumers) during four periods of the annual flood pulse. As stream conditions changed from high-water to low-water, we hypothesized that: 1) the piscivore-non-piscivore ratio would increase; 2) dietary diversity would decrease; 3) interspecific dietary overlap would decline; 4) fewer allochthonous food items would be consumed; and 5) food-web connectance would increase. The piscivore-non-piscivore abundance ratio was higher in both streams during the low-water period. Dietary diversity declined as water levels dropped and availability of aquatic habitats and resources declined, but interspecific dietary overlap was not lower. Contrary to our hypothesis, average interspecific dietary overlap increased at Charcote as the dry season progressed, even though dietary overlap among species was significantly lower than expected by chance. We did not find strong support for our hypotheses regarding seasonal patterns of consumption of allochthonous resources and food web connectance, both of which revealed little seasonal variation.(AU)

Redes alimentares não são entidades estáticas; interações entre consumidores e recursos variam no tempo e no espaço, o que complica as representações das estruturas de redes alimentares. Nós estimamos a estrutura da assembléia de peixes e dieta em dois riachos de água clara na região venezuelana dos Llanos (Charcote e Charcotico) e construímos redes tróficas (sub-redes definidas por peixes como os principais consumidores) para quatro períodos do pulso anual de inundação. À medida que as condições dos riachos mudam de águas altas para águas baixas, nós hipotetizamos que: 1) a razão piscívoros e não piscívoros irá aumentar; 2) a diversidade da dieta irá diminuir; 3) a sobreposição alimentar interespecífica irá diminuir; 4) menos itens alimentares alóctones serão consumidos; e 5) a conectância da teia alimentar irá aumentar. A razão da abundância de piscívoros e não piscívoros foi maior em ambos riachos durante a estação de águas baixas. A diversidade da dieta declinou à medida que as águas baixavam e a disponibilidade de habitats aquáticos e recursos declinavam, mas a sobreposição alimentar interespecífica não foi menor. Contrária à nossa hipótese, a média de sobreposição alimentar interespecífica aumentou no Charcote à medida que a estação cheia progrediu, mesmo com a sobreposição alimentar significativamente menor do que o esperado ao acaso. Não encontramos forte suporte para nossas hipóteses relacionadas aos padrões sazonais de consumo de recursos alóctones e conectância da cadeia trófica, os quais revelaram pouca variação sazonal.(AU)

MAP3K kinases and kidney injury / MAP3K quinasas y daño renal

Mitogen-activated protein kinases (MAP kinases) are functionally connected kinases that regulate key cellular process involved in kidney disease such as all survival, death, differentiation and proliferation. The typical MAP kinase module is composed by a cascade of three kinases: a MAP kinase kinase kinase (MAP3K) that phosphorylates and activates a MAP kinase kinase (MAP2K) which phosphorylates a MAP kinase (MAPK). While the role of MAPKs such as ERK, p38 and JNK has been well characterized in experimental kidney injury, much less is known about the apical kinases in the cascade, the MAP3Ks. There are 24 characterized MAP3K (MAP3K1 to MAP3K21 plus RAF1, BRAF and ARAF). We now review current knowledge on the involvement of MAP3K in non-malignant kidney disease and the therapeutic tools available. There is in vivo interventional evidence clearly supporting a role for MAP3K5 (ASK1) and MAP3K14 (NIK) in the pathogenesis of experimental kidney disease. Indeed, the ASK1 inhibitor Selonsertib has undergone clinical trials for diabetic kidney disease. Additionally, although MAP3K7 (MEKK7, TAK1) is required for kidney development, acutely targeting MAP3K7 protected from acute and chronic kidney injury; and targeting MAP3K8 (TPL2/Cot) protected from acute kidney injury. By contrast MAP3K15 (ASK3) may protect from hypertension and BRAF inhibitors in clinical use may induced acute kidney injury and nephrotic syndrome. Given their role as upstream regulators of intracellular signaling, MAP3K are potential therapeutic targets in kidney injury, as demonstrated for some of them. However, the role of most MAP3K in kidney disease remains unexplored

Las proteínas quinasas activadas por mitógenos (MAP quinasas) son quinasas conectadas funcionalmente que regulan procesos celulares clave involucrados en la enfermedad renal como la supervivencia, la muerte, la diferenciación y la proliferación. El típico módulo MAP quinasa está compuesto por una cascada de 3 quinasas: una MAP quinasa quinasa quinasa (MAP3K) que fosforila y activa una MAP quinasa quinasa (MAP2K) que, a su vez, fosforila una MAP quinasa (MAPK). Si bien el papel de las MAPK como ERK, p38 y JNK se ha caracterizado bien en las lesiones renales experimentales, se sabe mucho menos acerca de las quinasas apicales en la cascada, las MAP3K. Hay 24 MAP3K (MAP3K1 a MAP3K21, más RAF1, BRAF y ARAF). En este trabajo revisamos el conocimiento actual sobre la participación de MAP3K en la enfermedad renal no maligna y las herramientas terapéuticas disponibles. Existe evidencia intervencionista experimental in vivo que respalda claramente el papel de MAP3K5 (ASK1) y MAP3K14 (NIK) en la patogenia de la enfermedad renal experimental. De hecho, el inhibidor de ASK1, selonsertib, ha sido estudiado en ensayos clínicos en la enfermedad renal diabética. Además, aunque la MAP3K7 (MEKK7, TAK1) es necesaria para el desarrollo renal, la inhibición de MAP3K7 en el adulto protegió de la lesión renal aguda y crónica experimental; e inhibir MAP3K8 (TPL2/Cot) protegió de la lesión renal aguda. Por el contrario, MAP3K15 (ASK3) puede proteger de la hipertensión y los inhibidores de BRAF, en uso clínico, pueden inducir lesión renal aguda y síndrome nefrótico. Dado su papel como reguladores de los primeros pasos de la señalización intracelular, las MAP3K son posibles dianas terapéuticas en la lesión renal, como se ha demostrado para algunas de ellos. Sin embargo, el papel de la mayoría de las MAP3K en la enfermedad renal no ha sido explorado