Dear Rachel,
Here are some data to update the entry for Dichaete Specifically, the
statement in FBrf0075380; 'It is therefore unclear whether this lethality
represents a vital function for the wild type allele of D itself as opposed
to that of an adjacent gene.' is no longer correct. All of the lethal
dominant D alleles are lethal over the EMS induced point allele Dr72 and
the coding sequence deletion Dr513, indicating straightforward allelism.
Furthermore, all of the lethal dominant alleles have been characterised
with respect to the expression of Dichaete in the embryo, they all show
tissue-specific loss of Dichaete expression and thus are regulatory
mutations. The location of the breakpoints of each of the alleles is
listed below, where 0 is the translational start of Dichaete. The range
represents the uncertainty, thus D4 breaks in a restriction fragment
between -9.8 and -12 and so on.
T(2;3)D4	-9.8 to -12.4
In(3)D6		-6.5 to -9
T(2;3)D7	-16 to -18
In(3L)Dr8	-5.5 to -6.5
In(3L)D10	-21 to -24
There is some uncertainty in the designation of D1, D3 and D9 as dominant D
alleles The wing phenotype of the dominant alleles is due to ectopic
expression of Dichaete in the anlage of the hinge in the wing imaginal
disc, the phenotype can be reproduced by driving UASDichaete in the wing
hinge with the GAL4 drivers ms209 and 30A. both D3 and D9 are deletions of
the Dichaete transcription unit, phenotypically they behave as null alleles
when assayed in the embryo.
D3 is an additional abberation on top of the D1 chromosome which results in
the deletion of the 3' portion of the Dichaete transcription unit, it is a
protein null when assayed in whole mount embryos with anti-D antisera.
Since the wing phenotype of D3 is similar, if not identical to, D1 when
assayed in outcrossed individuals, these data raise the possibility that D1
itself is not due to Dichaete. Dichaete protein is ectopically expressed
in the wing discs of D1 individuals and reversion of D1 is associated with
loss of Dichaete in the wing disc. It is possible that the D1 and D3
inversions reflect dominant mutations in Sail.
D9 is a deletion which begins approximately 30 Kb 3' of the transcription
unit and extends proximal, removing the transcription unit. The cause of
the dominant phenotype in this case is not known.
Steve