Addendum to FBrf0222124(Xu et al., 2013)
We studied the DART1 loss-of-function allele DART150, an excision line
generated from P{SUPor-P}Art1KG09631, which was previously described for its
semi-penetrant phenotype during metamorphosis (Kimura et al., 2008). Among the
~10% of homozygous DART150/DART150 mutants that survive to adulthood, one third
showed an incomplete wing posterior crossvein (PCV), phenocopying a wing defect
previously reported for BMP pathway loss-of-function, e.g. in gbb and dpp
mutants (Khalsa et al., 1998; Stultz et al., 2005). The PCV defect in the
DART150/DART150 mutants correlated with the absence of phospho-Mad
immunoreactivity in part of the prospective PCV region of the developing pupal
wing, suggesting that lack of Mad activation underlies the DART150 phenotype.
We further examined whether DART1 genetically interacts with dpp signaling,
using the weak dpp allele dpps11, which exhibits wing venation defects when
crossed with other dpp loss-of-function alleles (Stultz et al., 2005). Indeed,
combining homozygous DART150 with heterozygous dpps11 resulted in the
shortening of the fifth longitudinal vein L5 in almost all flies, a venation
defect that was not seen in homozygous DART150 or dpps11 heterozygotes
alone. These data suggest a genetic interaction between DART1 and dpp signaling
in Drosophila, and are consistent with the effects of DART1 overexpression in
the suppression of Dad function in the wing disc (Xu et al., 2013). As a caveat
to the above experiments, the PCV phenotype and lethality were not seen in
genetic combination of DART150 with the deficiencies Df(3R)Exel6159,
Df(3R)Exel7305, Df(3R)ED5495, Df(3R)BSC479 or Df(3R)BSC529 that are reported to
delete the dart1 locus. On the other hand, the PCV phenotype and lethality
could not be outcrossed over eight generations using the P element
P{SUPor-P}KG05409, arguing in favor of their association with the lesion in
DART1. Also, PCR analysis confirmed a lesion in the DART1 locus as described
(Kimura et al., 2008). These findings may be consistent with a causative role
of the DART150 excision for the observed phenotypes and lethality, when
assuming additional genetic modifiers in nearby genomic regions.
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* Xu, J., Wang, A.H., Oses-Prieto, J., Makhijani, K., Katsuno, Y., Pei, M.,
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