Fig. 7: Proposed model for attachment defects leading to axonal degeneration. | Nature Communications

Fig. 7: Proposed model for attachment defects leading to axonal degeneration.

From: Epidermal control of axonal attachment via β-spectrin and the GTPase-activating protein TBC-10 prevents axonal degeneration

Fig. 7

a During normal body movement hemidesmosomes are mechanically resistant and attachment is maintained along the length of the axon in wild-type animals. In tbc-10;unc-70 mutants, these attachments are no longer mechanically resistant and the strain of movement leads to the intermittent loss of hemidesmosomes. Successive rounds of movement leads to increased local strain in the now detached axon, causing axonal breakage and degeneration. b Schematic representation of known and proposed components of hemidesmosomes linking the axons of touch receptor neurons to the epidermis. We propose that UNC-70/β-spectrin, the Rab-GTPase-activating protein TBC-10 and its RAB-35 target, maintain axonal integrity by functioning non-cell autonomously in the epidermis to control the stability of hemidesmosomes in response to mechanical strain via parallel pathways.

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