Cargo sorting and the subsequent membrane carrier formation require a properly organized endosomal actin network. To better understand the actin dynamics during endocytic recycling, we performed a genetic screen in C. elegans and identified RTKN-1/Rhotekin as a requisite to sustain endosome-associated actin integrity. Loss of RTKN-1 led to a prominent decrease in actin structures and basolateral recycling defects. Furthermore, we showed that the presence of RTKN-1 thwarts the actin disassembly competence of UNC-60A/cofilin. Consistently, in RTKN-1–deficient cells, UNC-60A knockdown replenished actin structures and alleviated the recycling defects. Notably, an intramolecular interaction within RTKN-1 could mediate the formation of oligomers. Overexpression of an RTKN-1 mutant form that lacks self-binding capacity failed to restore actin structures and recycling flow in rtkn-1 mutants. Finally, we demonstrated that SDPN-1/Syndapin acts to direct the recycling endosomal dwelling of RTKN-1 and promotes actin integrity there. Taken together, these findings consolidated the role of SDPN-1 in organizing the endosomal actin network architecture and introduced RTKN-1 as a novel regulatory protein involved in this process. 相似文献
Changes in invertebrate body size-distributions that follow loss of habitat-forming species can potentially affect a range of ecological processes, including predation and competition. In the marine environment, small crustaceans and other mobile invertebrates (‘epifauna') represent a basal component in reef food webs, with a pivotal secondary production role that is strongly influenced by their body size-distribution. Ongoing degradation of reef habitats that affect invertebrate size-distributions, particularly transformation of coral and kelp habitat to algal turf, may thus fundamentally affect secondary production. Here we explored variation in size spectra of shallow epifaunal assemblages (i.e. the slope and intercept of the linear relationship between log abundance and body size at the assemblage level) across 21 reef microhabitats distributed along an extensive eastern Australian climatic gradient from the tropical northern Great Barrier Reef to cool temperate Tasmania. When aggregated across microhabitats at the site scale, invertebrate body size spectra (0.125–8 mm range) were consistently log-linear (R2 ranging 0.87–0.98). Size spectra differed between, but not within, major groups of microhabitats, and exhibited little variability between tropical and temperate biomes. Nevertheless, size spectra showed significant tropical/temperate differences in slopes for epifauna sampled on macroalgal habitats, and in elevation for soft coral and sponge habitats. Our results reveal epifaunal size spectra to be a highly predictable macro-ecological feature. Given that variation in epifaunal size spectra among groups of microhabitats was greater than variation between tropical and temperate biomes, we postulate that ocean warming will not greatly alter epifaunal size spectra directly. However, transformation of tropical coral and temperate macroalgal habitats to algal turfs due to warming will alter reef food web dynamics through redistribution of the size of prey available to fishes. 相似文献
The imbalance between excess reactive oxygen species (ROS) generation and insufficient antioxidant defenses contribute to a range of neurodegenerative diseases. High ROS levels damage cellular macromolecules such as DNA, proteins and lipids, leading to neuron vulnerability and eventual death. However, the underlying molecular mechanism of the ROS regulation is not fully elucidated. Recently, an increasing number of studies suggest that microRNAs (miRNAs) emerge as the targets in regulating oxidative stress. We recently reported the neuroprotective effect of miR-137-3p for brachial plexus avulsion-induced motoneuron death. The present study is sought to investigate whether miR-137-3p also could protect PC12 cells against hydrogen peroxide (H2O2) induced neurotoxicity. By using cell viability assay, ROS assay, gene and protein expression assay, we found that PC-12 cells exposed to H2O2 exhibited decreased cell viability, increased expression levels of calpain-2 and neuronal nitric oxide synthase (nNOS), whereas a decreased miR-137-3p expression. Importantly, restoring the miR-137-3p levels in H2O2 exposure robustly inhibited the elevated nNOS, calpain-2 and ROS expression levels, which subsequently improved the cell viability. Furthermore, the suppressive effect of miR-137-3p on the elevated ROS level under oxidative stress was considerably blunted when we mutated the binding site of calpain-2 targted by miR-137-3p, suggesting the critical role of calpain-2 involving the neuroprotective effect of miR-137-3p. Collectively, these findings highlight the neuroprotective role of miR-137-3p through down-regulating calpain and NOS activity, suggesting its potential role for combating oxidative stress insults in the neurodegenerative diseases.