Kim, L. A. | bioRxiv Science

bioRxiv2025

In-vivo dendrite injury drives local mitochondrial contraction and dendrite branching

Mitochondria regulate cellular homeostasis in development and disease, and mitochondrial morphology plays a role in local injury signaling and wound repair. How mitochondria respond during dendrite injury remains an open fundamental question. Here we show that mitochondria contract rapidly and locally after laser dendrotomy. In the proximal intact dendrite, the extent of mitochondrial contraction diminishes with increasing distance from the injury site. We report that mitochondrial contraction is dependent on injury severity and that immediate contraction after injury results in a spatiotemporal increase in dendrite branching. Additionally, we find that mitochondrial contraction is inhibited by KCNJ2 (potassium inwardly rectifying channel subfamily J member 2), providing evidence that mitochondrial contraction is regulated by electrical activity. Mechanistically, we find that injury-induced mitochondrial contraction requires Drp1 (Dynamin related protein 1). In conclusion, these in-vivo findings characterize a dendrite response for mitochondria in neurons and provide insight into the regenerative outcomes of dendrites after injury. Graphical abstractIn-vivo dendrite injury drives local mitochondrial contraction and dendrite branching O_FIG O_LINKSMALLFIG WIDTH=175 HEIGHT=200 SRC="FIGDIR/small/658131v1_ufig1.gif" ALT="Figure 1"> View larger version (17K): org.highwire.dtl.DTLVardef@e4c767org.highwire.dtl.DTLVardef@1df4f23org.highwire.dtl.DTLVardef@1c4bf4aorg.highwire.dtl.DTLVardef@1ea9f76_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2017

Universal Transcriptional Responses to Different Modalities of Traumatic Stress as a Measure of Stress Exposure

Molecular diagnostic tools that can robustly and quantitatively measure the response to traumatic stress would be of considerable value in assessing the individual risk of developing post-traumatic stress disorder or stress-induced depression following stress exposure. The gene regulatory network can integrate and encode a large number of different signals, including those elicited by exposure to stress. We find that many genes respond to at least one modality of stress but only a subset of stress-sensitive genes track stress exposure across multiple stress modalities and are thus universal markers of stress exposure. A sensitive and robust measure of stress exposure can be constructed using a small number of genes selected from this modality-independent set of stress-sensitive genes. This stress-sensitive gene expression (SSGE) index can detect chronic traumatic stress exposure in a wide range of different stress models in a manner that is relatively independent of the modality of stress exposure and that parallels the intensity of stress exposure in a dose-dependent manner.

physiology↗