Decomposition of coarse woody debris in a long-term litter manipulation experiment: A focus on nutrient availability

The majority of above-ground carbon in tropical forests is stored in wood, which is returned to the atmosphere during decomposition of coarse woody debris. However, the factors controlling wood decomposition have not been experimentally manipulated over time scales comparable to the length of this process.We hypothesized that wood decomposition is limited by nutrient availability and tested this hypothesis in a long-term litter addition and removal experiment in a lowland tropical forest in Panama. Specifically, we quantified decomposition using a 15-year chronosequence of decaying boles, and measured respiration rates and nutrient limitation of wood decomposer communities.The long-term probability that a dead tree completely decomposed was decreased in plots where litter was removed, but did not differ between litter addition and control treatments. Similarly, respiration rates of wood decomposer communities were greater in control treatments relative to litter removal plots; litter addition treatments did not differ from either of the other treatments. Respiration rates increased in response to nutrient addition (nitrogen, phosphorus, and potassium) in the litter removal and addition treatments, but not in the controls.Established decreases in concentrations of soil nutrients in litter removal plots and increased respiration rates in response to nutrient addition suggest that reduced rates of wood decomposition after litter removal were caused by decreased nutrient availability. The effects of litter manipulations differed directionally from a previous short-term decomposition study in the same plots, and reduced rates of bole decomposition in litter removal plots did not emerge until after more than 6 years of decomposition. These differences suggest that litter-mediated effects on nutrient dynamics have complex interactions with decomposition over time

Mycobacterium marinum antagonistically induces an autophagic response while repressing the autophagic flux in a TORC1- and ESX-1-dependent manner.

Autophagy is a eukaryotic catabolic process also participating in cell-autonomous defence. Infected host cells generate double-membrane autophagosomes that mature in autolysosomes to engulf, kill and digest cytoplasmic pathogens. However, several bacteria subvert autophagy and benefit from its machinery and functions. Monitoring infection stages by genetics, pharmacology and microscopy, we demonstrate that the ESX-1 secretion system of Mycobacterium marinum, a close relative to M. tuberculosis, upregulates the transcription of autophagy genes, and stimulates autophagosome formation and recruitment to the mycobacteria-containing vacuole (MCV) in the host model organism Dictyostelium. Antagonistically, ESX-1 is also essential to block the autophagic flux and deplete the MCV of proteolytic activity. Activators of the TORC1 complex localize to the MCV in an ESX-1-dependent manner, suggesting an important role in the manipulation of autophagy by mycobacteria. Our findings suggest that the infection by M. marinum activates an autophagic response that is simultaneously repressed and exploited by the bacterium to support its survival inside the MCV

Durability of Radiofrequency Ablation in Barrett's Esophagus With Dysplasia

Radiofrequency ablation (RFA) can eradicate dysplasia and intestinal metaplasia in patients with dysplastic Barrett’s esophagus (BE), and reduce rates of esophageal adenocarcinoma. We assessed long-term rates of eradication, durability of neosquamous epithelium, disease progression, and safety of RFA in patients with dysplastic BE

The Cytosolic Sensor cGAS Detects Mycobacterium tuberculosis DNA to Induce Type I Interferons and Activate Autophagy.

Type I interferons (IFNs) are critical mediators of antiviral defense, but their elicitation by bacterial pathogens can be detrimental to hosts. Many intracellular bacterial pathogens, including Mycobacterium tuberculosis, induce type I IFNs following phagosomal membrane perturbations. Cytosolic M. tuberculosis DNA has been implicated as a trigger for IFN production, but the mechanisms remain obscure. We report that the cytosolic DNA sensor, cyclic GMP-AMP synthase (cGAS), is required for activating IFN production via the STING/TBK1/IRF3 pathway during M. tuberculosis and L. pneumophila infection of macrophages, whereas L. monocytogenes short-circuits this pathway by producing the STING agonist, c-di-AMP. Upon sensing cytosolic DNA, cGAS also activates cell-intrinsic antibacterial defenses, promoting autophagic targeting of M. tuberculosis. Importantly, we show that cGAS binds M. tuberculosis DNA during infection, providing direct evidence that this unique host-pathogen interaction occurs in vivo. These data uncover a mechanism by which IFN is likely elicited during active human infections