bioRxiv Science⌕ Search

Biology subjects

Davison, C. A.

Publications and source records attributed to Davison, C. A..

3 recordsLinked to original sources

Tubulin autoregulation factors SCAPER and TTC5 recruit γ-tubulin to non-centrosomal MTOCs for neuronal microtubule nucleation and axon regeneration

Neuronal function and survival depend on highly stereotyped non-centrosomal microtubule (MT) arrays. How these arrays form remains poorly understood. Here we identified a role for SCAPER and TTC5, two factors previously implicated in tubulin mRNA autoregulation, in controlling neuronal MT content through {gamma}-tubulin-dependent nucleation. In C. elegans neurons, loss of scpr-1, ttc-5, or both reduced MT numbers to a similar degree as depletion of {gamma}-tubulin, the main MT nucleator. Using conditional single-cell degradation alleles and endogenous tagging, we find that {gamma}-tubulin nucleates MTs in the neuronal cell body from endosomal puncta, and that scpr-1 and ttc-5 are required to recruit {gamma}-tubulin to these structures. SCPR-1 is also instructive, as its overexpression drastically increases {gamma}-tubulin levels and enhances MT density. We propose that these mechanisms are conserved since human SCAPER rescues C. elegans mutants, and SCAPER knockdown in rat hippocampal neurons reduces both {gamma}-tubulin clustering at presynaptic sites and activity-dependent synaptic MT nucleation. Finally, while scpr-1, ttc-5, and{gamma} -tubulin are not required for developmental axon elongation, they are essential for regeneration, where SCPR-1 directs {gamma}-tubulin to the growth cone to facilitate regrowth following injury. These findings reveal mechanisms governing neuronal cytoskeleton assembly and function, and suggest potential crosstalk between tubulin autoregulation and microtubule nucleation.

cell biology↗

The neuron-intrinsic membrane skeleton is required for motor neuron integrity throughout lifespan

Axons experience physical stress throughout an organisms lifetime, and disruptions in axonal integrity are hallmarks of both neurodegenerative diseases and traumatic injuries. The spectrin-based membrane periodic skeleton (MPS) is proposed to have a crucial role in maintaining axonal strength, flexibility, and resilience. To investigate the importance of the intrinsic MPS for GABAergic motor neuron integrity in C. elegans, we employed the auxin-inducible degron system to degrade {beta}-spectrin/UNC-70 in a cell-type specific and time-dependent manner. Degradation of {beta}-spectrin from all neurons beginning at larval development resulted in widespread axon breakage and regeneration in VD/DD GABAergic motor neurons in both larval and adult animals. Similarly, targeted degradation of {beta}-spectrin in GABA neurons alone resulted in extensive breakage. Moreover, we found that depleting {beta}-spectrin from the mature nervous system also induced axon breaks. By contrast, epidermal {beta}-spectrin was not required for axon integrity of VD/DD neurons. These findings demonstrate the cell-intrinsic importance of neuronal {beta}-spectrin/UNC-70 for axon integrity both during development and in adulthood.

neuroscience↗

A functional non-coding RNA is produced from xbp-1 mRNA

The xbp-1 mRNA encodes the XBP-1 transcription factor, a critical part of the unfolded protein response. Here we report that an RNA fragment produced from xbp-1 mRNA cleavage is a biologically active non-coding RNA (ncRNA) in Caenorhabditis elegans neurons, providing the first example of ncRNA derived from mRNA cleavage. We show that the xbp-1 ncRNA is crucial for axon regeneration in vivo, and that it acts independently of the protein-coding function of the xbp-1 transcript. Structural analysis indicates that the function of the xbp-1 ncRNA depends on a single RNA stem; and this stem forms only in the cleaved xbp-1 ncRNA fragment. Disruption of this stem abolishes the non-coding but not coding function of the endogenous xbp-1 transcript. Thus, cleavage of the xbp-1 mRNA bifurcates it into a coding and a non-coding pathway; modulation of the two pathways may allow neurons to fine-tune their response to injury and other stresses. Graphic abstract O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY

neuroscience↗