The Deadbeat Paternal Effect of Uncapped Sperm Telomeres on Cell Cycle Progression and Chromosome Behavior in Drosophila melanogaster.

Telomere-capping complexes (TCCs) protect the ends of linear chromosomes from illegitimate repair and end-to-end fusions and are required for genome stability. The identity and assembly of TCC components have been extensively studied, but whether TCCs require active maintenance in nondividing cells remains an open question. Here we show that Drosophila melanogaster requires Deadbeat (Ddbt), a sperm nuclear basic protein (SNBP) that is recruited to the telomere by the TCC and is required for TCC maintenance during genome-wide chromatin remodeling, which transforms spermatids to mature sperm.

Rel A/p65 is required for cytokine-induced myotube atrophy.

Muscle atrophy can be triggered by systemic illnesses that are associated with elevated proinflammatory/catabolic cytokines, which, in turn, are thought to contribute to muscle wasting. In this study, we found that the prototypical NF-κB transcription factor, Rel A (p65), is required for NF-κB activation in C2C12 and L6 myotubes due to treatment with exogenous TNF-α, IL-1α, IL-1β, TNF-related weak inducer of apoptosis, but not IL-6. All five cytokines induced atrophy in C2C12 myotubes, and inhibition of p65 reversed atrophy due to TNF-α, IL-1α, IL-1β, TNF-related weak inducer of apoptosis, but not IL-6 treatment.