Predation of Caiman yacare (Spix, 1825) (Crocodilia, Alligatoridae) by Busarellus nigricollis (Latham, 1790) (Accipitriformes, Accipitridae) in the Taiama Ecological Station, Alto Pantanal, State of Mato Grosso

Predation of Caiman yacare (Spix, 1825) (Crocodilia, Alligatoridae) by Busarellus nigricollis (Latham, 1790) (Accipitriformes, Accipitridae) in the Taiama Ecological Station, Alto Pantanal, State of Mato Grosso. The Black-collared Hawk Busarellus nigricollis is an Accipitridae commonly seen on river banks, lagoon shores, and marshy areas. It feeds mainly on fishes and aquatic insects. It hunts from dead tree branches at forest edges or emergent trunks in flooded areas. Detailed information about the Black-collared Hawk food habits is scarce. In this study, we describe the predation of Caiman yacare (Pantanal alligator) by an individual of B. nigricollis. The event was observed on 20 August 2010 at 10: 14 am, in the Taiama Ecological Station, municipality of Caceres, Alto Pantanal, state of Mato Grosso. The B. nigricollis individual was seen leaving the Paraguay River carrying a juvenile C. yacare around 40 cm long. The prey was torn apart and given to a Black-collared Hawk nestling sitting atop a nest in flooded forest, ca. 15 m way from the river bank. This is the first published record of Pantanal alligator predation by the Black-collared Hawk.

Mutations in ADAR1 cause Aicardi-Goutieres syndrome associated with a type I interferon signature

Adenosine deaminases acting on RNA (ADARs) catalyze the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) and thereby potentially alter the information content and structure of cellular RNAs. Notably, although the overwhelming majority of such editing events occur in transcripts derived from Alu repeat elements, the biological function of non-coding RNA editing remains uncertain. Here, we show that mutations in ADAR1 (also known as ADAR) cause the autoimmune disorder Aicardi-Goutieres syndrome (AGS). As in Adar1-null mice, the human disease state is associated with upregulation of interferon-stimulated genes, indicating a possible role for ADAR1 as a suppressor of type I interferon signaling. Considering recent insights derived from the study of other AGS-related proteins, we speculate that ADAR1 may limit the cytoplasmic accumulation of the dsRNA generated from genomic repetitive elements.