An Antimicrobial Peptide and Its Neuronal Receptor Regulate Dendrite Degeneration in Aging and Infection.

Infections have been identified as possible risk factors for aging-related neurodegenerative diseases, but it remains unclear whether infection-related immune molecules have a causative role in neurodegeneration during aging. Here, we reveal an unexpected role of an epidermally expressed antimicrobial peptide, NLP-29 (neuropeptide-like protein 29), in triggering aging-associated dendrite degeneration in C. elegans.

DAPK interacts with Patronin and the microtubule cytoskeleton in epidermal development and wound repair.

Epidermal barrier epithelia form a first line of defense against the environment, protecting animals against infection and repairing physical damage. In death-associated protein kinase (DAPK-1) regulates epidermal morphogenesis, innate immunity and wound repair. Combining genetic suppressor screens and pharmacological tests, we find that DAPK-1 maintains epidermal tissue integrity through regulation of the microtubule (MT) cytoskeleton.

Image registration robust to sparse large errors.

Registration is difficult when images to be registered contain sparse but large-valued differences. We present a method for robust registration that ignores some fraction of large differences, while constraining the sparseness of these errors. We apply the method to stabilize microscopy videos of C.

Axon injury triggers EFA-6 mediated destabilization of axonal microtubules via TACC and doublecortin like kinase.

Axon injury triggers a series of changes in the axonal cytoskeleton that are prerequisites for effective axon regeneration. In Caenorhabditis elegans the signaling protein Exchange Factor for ARF-6 (EFA-6) is a potent intrinsic inhibitor of axon regrowth. Here we show that axon injury triggers rapid EFA-6-dependent inhibition of axonal microtubule (MT) dynamics, concomitant with relocalization of EFA-6.

The microtubule minus-end-binding protein patronin/PTRN-1 is required for axon regeneration in C. elegans.

Precise regulation of microtubule (MT) dynamics is increasingly recognized as a critical determinant of axon regeneration. In contrast to developing neurons, mature axons exhibit noncentrosomal microtubule nucleation. The factors regulating noncentrosomal MT architecture in axon regeneration remain poorly understood.

Insights into the functions of the death associated protein kinases from C. elegans and other invertebrates.

The death associated protein kinases (DAPK) are a phylogenetically widespread family of calcium-regulated serine/threonine kinases, initially identified from their roles in apoptosis. Subsequent studies, principally in vertebrate cells or models, have elucidated the functions of the DAPK family in autophagy and tumor suppression. Invertebrate genetic model organisms such as Drosophila and C.