Forward and backward movement are both affected, but the forward
Unc phenotype is more severe.
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).
Eight animals displayed a severe backward
Unc phenotype but were still capable of forward locomotion, confirming that AVAs had been properly ablated.
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
Broods from these animals grown at 15 °C were later examined for the presence of any animals displaying a kinker (
Unc -124-like)
phenotype.
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).
The
phenotype of
unc - 9
unc - 7 double mutants is no more severe than either single mutant
phenotype, consistent with the co-localization of
UNC - 9:: GFP and
UNC - 7S.
The focus of action of the e1500 rubberband
phenotype is the body wall muscles — when the sup - 10 (+) free duplication mnDp3 is present in body wall muscles, the animals have a rubberband
phenotype due to
unc - 93.
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 phenoty
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 phenoty
Unc - 7
phenotype.
The
phenotype of
unc - 9 daf - 6
unc - 7 mutants was no more severe than
unc - 7 alone, consistent with
UNC - 7 and
UNC - 9 acting in the same process.
Since
unc - 7 encodes a gap junction protein, we presumed that the mutant Unc - 7 uncoordinated phenotype reflects a loss of functional gap junction channe
unc - 7 encodes a gap junction protein, we presumed that the mutant
Unc - 7 uncoordinated phenotype reflects a loss of functional gap junction channe
Unc - 7 uncoordinated
phenotype reflects a loss of functional gap junction channels.
Although the focus of action of
unc - 9 can not be precisely determined from these mosaic experiments, the results are consistent with the interpretation that loss of unc - 9 (+) function from the P1 lineage can be tolerated without apparent effects on locomotion, and that the loss of unc - 9 (+) function from within the AB lineage gives rise to the Unc - 9 phenoty
unc - 9 can not be precisely determined from these mosaic experiments, the results are consistent with the interpretation that loss of
unc - 9 (+) function from the P1 lineage can be tolerated without apparent effects on locomotion, and that the loss of unc - 9 (+) function from within the AB lineage gives rise to the Unc - 9 phenoty
unc - 9 (+) function from the P1 lineage can be tolerated without apparent effects on locomotion, and that the loss of
unc - 9 (+) function from within the AB lineage gives rise to the Unc - 9 phenoty
unc - 9 (+) function from within the AB lineage gives rise to the
Unc - 9 phenoty
Unc - 9
phenotype.
unc - 93 (e1500) confers a gain - of - function rubberband
phenotype that is suppressed by the recessive sup - 10 (mn219) mutation.