Therefore, the Unc - 7 locomotory defect reflects loss of unc - 7 gap junction channel function, regardless of
ectopic gap junction formation, and we sought to determine which gap junctions in the nervous system include UNC - 7 as a component.
However, partial EM reconstruction of an unc - 7 (e5) mutant revealed
ectopic gap junctions formed between AVA interneurons that direct backward movement and B class motor neurons involved in forward movement.
The cause of the Unc phenotype is unknown but could be due to loss of functional gap junctions or to extra
ectopic gap junctions established between AVA interneurons and B motor neurons, noted in EM serial sections of an unc - 7 (e5) animal (White et al., personal communication, originally cited in [9]; Figure 1).
With respect to UNC - 7S co-localization, this indicated that UNC - 9 could potentially contribute subunits to hemichannels in the motor neurons, in AVB, or in both, and UNC - 9 may play a role in the formation of
ectopic gap junctions noted in unc - 7 (e5)(between AVA and B class motor neurons).
If
ectopic gap junctions are the sole cause of the Unc - 7 phenotype, then laser ablation of AVAs should eliminate communication between these interneurons and the B motor neurons and restore normal forward locomotion; in conjunction with AVA ablation, animals should be backward Unc (Figure 1).
Therefore, part of the characterization of the Unc - 7 phenotype involves understanding how
ectopic gap junction channels arise in the absence of the UNC - 7 innexin, and whether or not these ectopic neuronal connections contribute to the Unc phenotype.
Not exact matches
The AVA interneurons in ten unc - 7 (e5) L1 animals were then targeted; none displayed improvement in forward locomotion, supporting the conclusion that
ectopic AVA: B
gap junctions are not the sole cause of the Unc - 7 phenotype.
One hypothesis for unc - 7 uncoordination is that
ectopic AVA: B motor neuron
gap junctions interfere with forward locomotion.