Mutation in a gene can cause a change in sexual behaviour of fruitflies
RECENT research on a genetic mutation
in Drosophila melanogaster, commonly
known as vinegar fly or fruit fly, has
thrown new light on its effect on sexual
orientation. This mutation, initially discovered more than 30 years ago, was
found to convert normal heterosexual
males into bisexuals. These males
courted both males and females, seemingly with equal avidity. The mutant
gene was designated fruity, or fru, a
name that was subsequently changed to
fruitless. (Variant forms of the fru gene
that occur on the same chromosome, or
its alleles, exhibit homosexual, fertile
bisexual and sterile bisexual behaviour;
for the moment, it shall be assumed that
fertile bisexuals are being talked about.)
Daisuke Yamamoto and her team at
Mitsubishi Kasei Institute, Tokyo, have
now identified the possible reason for
this change in sexual orientation
(Proceedings of the us National Academy
of Sciences, Vol 93, 1996).
Yamamoto and her team started out
by mutagenesing fly stocks by making
use of a technique known as transposon
insertion. In this method, a mutation is
induced at random via the insertion of a
transposable element or 'jumping gene'
somewhere into the DNA of a host
organism. If the mutation happens to be
of the desired class - something that
can be decided by examining the form
or behaviour of the fly - it is an easy
matter to pick out the region Of DNA into
which the transposon has integrated; in
other words, to pick out the gene that
has been mutated.
The screenino procedure consisted
of observing the behaviour of single
male-female pairs of putative mutants
when they were thrown together. Seven
mutations were isolated. All were recessive: two copies of the mutated gene
were essential for a defect to be seen. A
single normal (wild-type) copy was suf-
ficient to override the mutant effect.
One of the mutants was named satori or
sat, the Japanese word for nirvana. It
was observed that mutant sat males did
not show any interest in normal (wild-
type) females. However, sat females are
indistinguishable in their courtship
behaviour from normal females. Therefore the
normal sat gene in some manner mediates the
courtship response of Drosophila males.
Unlike the fru mutant,
mutant sat males were
merely disinterested, not
bisexual. So it seemed
plausible that the two were
different genes. But when
the flies were cross-bred,
in order to generate males
that contained a' single
copy each of the fru and
sat mutations, it was
found that they were
bisexual ' Thefirulsat males
mated with females and
were fertile. It implied that the fru and
sat were two Mutations of different sorts
within the same gene. If they were
entirely different genes, as was assumed
earlier, the fru and sat mutations would
have been compensated for by the corresponding wild-type genes. This
hypothesis is supported by the observation that
both frulfru and sadsat males lack a pair
of sex-specific muscles in the abdomen.
In short, sat and fru are alleles Of
the same gene.
There are two possible explanations
to the functioning of the normal fruitless
gene (or satori, which is the same gene).
One, the fruitless DNA sequence encodes
a protein with characteristics that
resemble those of other DNA-binding
proteins that are known to be involved
in the pathway of sexual determination
in Drosophila.
Second, the fruitless gene was found
to be transcribed in two regions of the
brain: the mushroom body and the
antermal lobe. The latter might be
involved in neural processing of smells
that are used in sexual recognition. The
developmental failure ofthe sex-specific
muscle can be explained as being caused
by a defect in the nerves that enervate
the muscle. The hypothesis is that a failureto perceive odour cues, or an incorrect interpretation of odour cues, might
affect the courtship behaviour displayed
by fruitless males. Mutations in a single
sex-determination gene could lead to a
change in some brain cells and alter sexual orientation in the male.
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