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Fig. 7
lh3 in Peripheral Glia Rescues lh3 Dorsal Axon Regeneration Defects
(A–E) Pre-lesion (A) and 48 hpt (B) examples reveal that expression of lh3 in all muscles Tg(aActin:lh3mkate) fails to rescue lh3 axon regeneration. In contrast, pre-lesion (C) and 48 hpt (D) examples demonstrate that transgenic expression of lh3 in peripheral glia Tg(sox10:lh3mkate) significantly rescued these guidance defects (E).
(F) After nerve transection, regenerating motor axons cross the injury gap to return to distal Schwann cells and reinnervate dorsal muscle targets. lh3 glycosylation of ECM components and the lh3 substrate col4a5 are required for targeting dorsal, but not ventral, motor axon regeneration. Col4a5 is upregulated in ventral and ventrolateral Schwann cells where it may act to present canonical guidance cues, such as slit1a, to destabilize regenerating axons. Dashed white boxes outline the nerve transection site; dashed yellow triangle, dorsal ROI; red arrowheads, aberrant regrowth; scale bar, 10 µm.