Biology Reference
In-Depth Information
early cell cycle 14, ending when somatic cells first form in the young embryo.
As this promoter shuts off, the second promoter,
Sxl
Pm
, comes on in both sexes.
However, because the transcripts from this promoter require full-length SXL pro-
tein to remove a male-specific exon, only the expression of the
Sxl
Pm
in females
generates messenger RNAs (mRNAs) that encode the full-length SXL protein.
Thus, the earliest
Sxl
+
transcripts differ from later transcripts and male tran-
scripts are inactive because they include an extra exon that stops the transla-
tion process. Initiation of
Sxl
+
expression requires the action of genes from the
mother (maternal genes such as
da
+
,
her
+
,
emc
+
, and
gro
+
) (
Figure 10.2
). In
males, the
Sxl
+
master gene is OFF, and the four
male-specific lethal
+
autosomal
genes are ON, a combination that leads to male somatic-sexual differentiation
and hypertranscription of the single X chromosome (
Figure 10.1
).
Maternal-effect genes influence the development of progeny, as discussed
in Chapter 4. Maternal-effect genes function in one of two ways: either the
mother produces a gene product that is transferred into and stored in the egg,
or the mother's messenger RNA is transferred into and stored in the eggs and
subsequently is translated by the embryo. At least four maternal X:A signal-
transduction genes have been found, including
daughterless
+
(
da
+
),
hermaph-
rodite
+
(
her
+
),
extramachrochaetae
+
(
emc
+
), and
groucho
+
(
gro
+
) (
Figure 10.1
,
Table 10.1
). Female progeny of mothers with mutant forms of
da
+
fail to acti-
vate the key master gene
Sxl
+
and die as embryos. Male progeny of
da
mothers
survive because they do not require
Sxl
+
.
Sxl
+
is the master switch gene involved in both sex determination and dos-
age compensation in
D
.
melanogaster
. It regulates pre-mRNA splicing for itself
and for
transformer
+
(
tra
+
) and
male-specific-lethal-2+
+
(
msl-2
+
). Once
Sxl
+
is ON
in females, a second series of regulatory genes are important in differentiating
between the alternative pathways in somatic cell development. These secondary
switch genes include
transformer
+
(
tra
+
),
transformer-2
+
(
tra-2
+
),
intersex
+
(
ix
+
),
doublesex
+
(
dsx
+
), and
fruitless
+
(
fru
+
) (
Figure 10.2
). Mutations of
tra
+
,
tra-2
+
,
and
ix
+
affect somatic-sex determination in females, but are not needed for male
somatic differentiation (
Table 10.1
). In the absence of TRA proteins in males,
the
fruitless
+
gene transcript affects as many as 500 neurons in the brain (
Figure
10.2
), which regulates male sexual behavior and also affect the male-specific
muscle (Muscle of Lawrence, MOL) used in mating. Although
tra-2
+
is not needed
for male differentiation, it is critical for normal spermatogenesis in males.
The
doublesex
+
locus is needed for differentiation of both male and female
external morphology (
Figure 10.2
). The
dsx
+
gene is a
double switch
, with
only one switch functioning in a particular sex. When
dsx
+
is active in males
