achaete
Achaete protein first accumulates in the neuroectoderm in segmentally repeated clusters of 5 to 7 ectodermal cells in late stage 8. Two medial and two later clusters are found per hemisegment. One cell in each cluster comes to express achaete most intensely, and the future neuroblast delaminates. Next, the remaining cells lose achaete expression. Once the neuroblast has delaminated, and before it undergoes any divisions, ac expression in the neuroblast is extinguished. Thus four ac-positive cells on each side of the hemisegment delaminate and form a neuroblast. Only four of the first 10 neuroblasts express achaete. Neurogenic genes, including Notch and Delta, suppress ac expression in the non-segregating cells of each proneural cluster (Skeath, 1992a).
intermediate neuroblasts defective mutations were isolated by a mutagenesis screen for altered even-skipped (eve) expression in the CNS (J. Skeath and C.Q. Doe, unpubl.). The earliest ind mutant phenotype is observed in stage 7 embryonic neuroectoderm, when muscle segment homeobox expression occurs both in its normal locations in the dorsal columns and in the adjacent intermediate columns. Thus ind represses transcription of msh directly or indirectly within intermediate column neuroectoderm. Normally the ind and msh expression domains are adjacent but nonoverlapping, consistent with negative regulation of msh by ind. During the earliest stage of neurogenesis (stage 8 of development), wild-type embryos show expression of the proneural gene achaete in rows 3 and 7 of the neuroectoderm, with expression restricted to the ventral and dorsal columns and excluded from the intermediate column. ind expression in the intermediate column precisely abuts these clusters of achaete-expressing cells without overlapping them. In ind mutant embryos, derepression of achaete expression is observed within the intermediate column of neuroectoderm in rows 3 and 7 . This is consistent with a transformation of
intermediate to dorsal neuroectoderm msh marker. It is concluded that ind represses
msh and achaete gene expression directly or indirectly, and that ind is necessary for establishing proper intermediate-column identity within the neuroectoderm (Weiss, 1998).
The proneural genes achaete and scute and the segment polarity genes wingless and engrailed each have limited expression in only a few identifiable and stereotyped clusters of the head. For example, sc appears exclusively in a small part of the protocerebral domain, followed by transient expression in one to two protocerebral neuroblasts. wg is expressed in a total of three patches and engrailed is expressed in domains that are posterior and ventral to the adjacent wg domains. en is expressed in one patch in both the protocerebrum and the deuterocerebrum (Younossi-Hartenstein, 1996).
Loss of function mutations of the achaete-scute complex lead to a
significant reduction of sensory bristles and glial cells. Genes within the complex affect gliogenesis
with different strength and display some functional redundancy. Thus, neurogenesis and gliogenesis
share the same genetic pathway. Despite these similarities, however, the mechanism of action of the
achaete-scute complex seems to be different in the two processes. Neural precursors express
products of the complex, therefore the role of these genes on neurogenesis is direct. However,
markers specific to glial cells do not colocalize with products of the achaete-scute complex, showing
that the complex affects gliogenesis indirectly. These observations lead to the hypothesis that
gliogenesis is induced by the presence of sensory organ cells, either the precursor or its progeny (Giangrande, 1995).
Embryonic expression of achaete is also found in neural precursor cells of the gnathal region of the head: specifically, the procephalic region, the optic lobe, the clypeolabrum, and the stomodeum (Romani, 1987).
Achaete is required for the formation of the stomatogastric nervous system (SNS). The SNS consists of several peripheral ganglia which receive input from the brain and in turn innervate the muscles, pharynx, and gut. Precursors originate from the primordium of the foregut or stomodeum [Images]. Several subsets of precursors delaminate from the stomodeal epithelium as individual cells early in development. At later stages these precursors migrate to various locations where they differentiate as neurons. The function of achaete-scute and neurogenic genes is identical here to their function in the development of the ventral nerve cord (Hartenstein, 1996).
Defects in single minded mutants are characterized
by the loss of the gene expression required for the proper formation of the ventral neurons and epidermis, and by a decrease in the spacing of longitudinal and commissural axon tracks. Molecular and cellular mechanisms for these defects
were analyzed to elucidate the precise role of the CNS midline cells in proper patterning of the ventral neuroectoderm during embryonic neurogenesis. These analyses have shown that the ventral neuroectoderm in the sim mutant fails to carry out its proper formation and characteristic cell division cycle. This results in the loss of the dividing neuroectodermal cells
that are located ventral to the CNS midline. The CNS midline cells are also required for the cell cycle-independent expression of the neural and epidermal markers. This indicates that the CNS midline cells are essential for the
establishment and maintenance of the ventral epidermal and neuronal cell lineage by cell-cell interaction. Nevertheless, the CNS midline cells do not cause extensive cell death in the ventral neuroectoderm. This study indicates that the
CNS midline cells play important roles in the coordination of the proper cell cycle progression and the correct identity determination of the adjacent ventral neuroectoderm along the dorsoventral axis (Chang, 2000).
sim is required for the proper development
of ventral epidermis. This was demonstrated by the fact that the
expression of the ventral ectodermal markers, enhancer
trap line BP28 and otd and pnt genes, is missing in the
sim mutant. Thus, this study focuses on
the role of the CNS midline cells in the formation and
identity determination of the ventral NBs during early
neurogenesis. Initial NB formation and identity determination
depend on the function of the achaete-scute
(ac-sc) complex of proneural genes to provide a group of
neuroectodermal cells with the competence to become a
NB. To investigate whether the CNS midline cells affect the
expression of a proneural gene that is essential for the
initial NB formation and identity determination, ac
expression pattern was analyzed by in situ hybridization.
In wild-type stage 9 embryos, ac is expressed in the MP2
and S1 NBs 3-5, 7-1, and 7-4 in each hemisegment. In sim embryos, ac expression is absent in more than
90% of the examined hemisegments. This result indicates
that the CNS midline cells are required for the
expression of the proneural genes in the medial and
lateral S1 NBs from the initial stage of neurogenesis (Chang, 2000).
Many gene networks used by developing organisms have been conserved over long periods of evolutionary time. Why is that? A model is presented of the core neurogenic network in Drosophila. This model exhibits at least three
related pattern-resolving behaviors that the real neurogenic network accomplishes during embryogenesis in Drosophila. Furthermore, the model exhibits these behaviors across a wide range of parameter values, with most of its parameters able to vary more than an order of magnitude while it still successfully forms these test patterns. With a single set of parameters, different initial conditions (prepatterns) can select between different
behaviors in the network's repertoire. Two new measures are introduced for quantifying network robustness that mimic recombination and allelic divergence and these were used to reveal the shape of the domain in the parameter space in which the model functions. Lateral inhibition yields robustness to changes in prepatterns and a reconciliation of two divergent sets of experimental results is suggested. Finally, it is shown that, for this model, robustness confers functional flexibility. It is concluded that the neurogenic network is robust to changes in parameter values, which gives it the flexibility to make new patterns. The model also offers a possible resolution of a debate on the role of lateral inhibition in cell fate specification (Meir, 2002).
The experimental literature includes both support for, and refutation of, an important role for lateral inhibition in neural determination. The results of this analysis can account for both sets of experiments. If the prepattern that initiates neuroblast selection is well tuned, the prepattern plus a constant level of inhibition could select the winner, absent lateral inhibition. But lateral inhibition buffers the patterning against perturbations in the initial prepatterning (e.g., due to genetic or environmental variation, or 'developmental noise'). Seugnet (1997) reported that, with only constant production of Dl, 80% of proneural clusters developed normally, but 20% produced an extra NB. These experiments are interpreted to say that the prepattern is well tuned in most proneural clusters, but in 20%, either a poorly tuned prepattern or noise causes errors in the absence of lateral inhibition. This is a testable idea. One could remove lateral inhibition as Seugnet did. It would then be predicted that the embryo would be much more sensitive to hyper- and hypo-morphs in prepatterning genes such as extramachrochaete and hairy. It would also be predicted that such embryos would be more sensitive to mutations in genes within the network itself, such as missing or extra copies of Dl or N. The latter prediction is made because those mutations should change the threshold to which the prepattern is tuned. In the absence of lateral inhibition, a prepattern that was well tuned to the former threshold could not also be well tuned to the new threshold (Meir, 2002).
From these results, it is deduced that E(spl) greatly reduces the percentage of random parameter sets that enable lateral inhibition. It is believed this is because E(spl) acts as a homeostat. As the expression levels of the proneural genes (ac and sc) rise, their products activate E(spl). E(spl) then downregulates the proneural genes. As with the thermostat in a house, this negative feedback loop tends to keep the proneural genes at an intermediate level rather than allowing them to switch to either a high or low state. Both E(spl) autoinhibition, and to a lesser extent cis-Dl inhibition of N activation, help overcome this homeostat. On the face of it, this seems a strange design. The ac/sc network itself is a bistable switch that tends to go in the direction it is pushed and remain there. The switch and homeostat mechanisms are exact opposites. Removing the homeostat (the reduced model) makes it easier to find parameter sets that pass various tests (which all involve throwing the switch). Why incorporate counteracting mechanisms in the same circuit (Meir, 2002)?
It is, of course, possible that this is simply a vestige of the network's evolutionary history, with no design rationale. But electrical engineering suggests one possible advantage. An op-amp is a famous circuit that amplifies the difference between two inputs. Good op-amps can amplify a voltage difference more than a million-fold. Usually, though, engineers add a negative feedback circuit (that is, a homeostat). This greatly attenuates the gain but makes the amplifier much more stable; noise generated internally inside the op-amp will not affect the output signal. Reducing function to gain stability is common in other electrical circuits as well. These electrical circuits do not make good direct analogies to genetic networks, but the concept of adding negative feedback to increase stability might still apply. Perhaps the E(spl) homeostat reduces the network's sensitivity to developmental noise such as stochastic changes in transcription or translation rates, in the prepattern, or in the concentrations of modulators such as Da and Emc (Meir, 2002).
A related design benefit might be that the E(spl) homeostat prevents the network from switching individual cells on or off before the prepattern has a chance to decree the winner. A simple bistable switch consisting of ac and sc alone could not help but be thrown in one direction or the other by noise (as apparently takes place in C. elegans anchor cell specification). Adding E(spl) leads to a new, neither-on-nor-off steady state, which could enable the proneural switch to procrastinate until some extrinsic cue forces the system to choose one or the other switched state (Meir, 2002).
Both Achaete and Scute accumulate in well defined proneural clusters in imaginal discs. Their expression patterns largely overlap (Gomez-Skarmeta, 1995).
The spatial organization of epidermal structures in the embryo and adult fly
constitutes a classicically modelled system for understanding how the two dimensional arrangement of
particular cell types is generated. Adult legs are
covered with sensory bristles, arranged in longitudinal rows in most segments. Two regulatory genes, hairy andachaete are chiefly responsible for setting up this periodic bristle pattern.
achaete is expressed during pupal leg development in a dynamic pattern that develops into narrow longitudinal stripes, 3-4 cells in width, each of which represents a field of cells (proneural field) from which bristle precursor
cells are selected. This pattern of gene expression foreshadows the adult bristle pattern
established in part through the function of the hairy gene.
In pupal legs, hairy is expressed in four longitudinal stripes, located between
every other pair of achaete stripes. In the absence of hairy function, achaete
expression expands into the interstripe regions that normally express hairy, fusing the two achaete
stripes and resulting in extra-wide stripes of achaete expression. This misexpression of achaete alters the fields of potential bristle precursor cells. This leads to the misalignment of bristle rows in the adult. hairy's role in patterning achaete expression is distinct from that in the
wing, in which Hairy suppresses late expression of achaete but has no effect on the initial patterning
of achaete expression. Thus, the leg bristle pattern is apparently regulated at two levels: a global
regulation of hairy and achaete expression patterns partitioning the leg epidermis into striped zones, and later, a local regulation that involves refinement steps that may control the alignment and spacing of bristle cells within these zones (Orenic, 1993).
Loss of function in genes of the achaete-scute complex causes neural hypoplasia (too few cells). A lower than normal proportion of neuroblasts delaminate from the neuroectoderm and there is increased cell death at later stages. Increasing the copy number of AS-C alleles leads to an opposite effect: neural hyperplasia (Jimenez, 1990). Note that the effect of mutation and overexpression of proneural genes is exactly the opposite of that observed with the neurogenic genes Delta and Notch.
Early in development the Drosophila endoderm segregates into three non-neural cell types: the principle midgut epithelial
cells, the adult midgut precursors, and the interstitial cell precursors. This process requires proneural and neurogenic genes. In
neurogenic mutants the principle midgut epithelial cells are missing and the other two cell types
develop in great excess. Consequently, the midgut epithelium does not form. In achaete-scute
complex and daughterless mutants the interstitial cell precursors do not develop and the number of
adult midgut precursors is strongly reduced. Development of the principle midgut epithelial cells and
formation of the midgut epithelium is restored in neurogenic proneural double mutants. The
neurogenic/proneural genes, in contrast to the neuroectoderm, are not expressed in small clusters of cells but initially homogeneously in the endoderm suggesting that no prepattern exists which
determines the position of the segregating cells (Tepass, 1995).
To test whether proneural genes not normally expressed in a specific precursor can function in the specification of neural precursor identity in the CNS, proneural proteins not normally expressed in the MP2 precursor cell were ectopically expressed in MP2 precursors. Unlike other CNS precursors, MP2 normally expresses achaete and scute only. MP2 is unique in several respects: in its localization of Prospero protein to the nucleus soon after delamination, in the subsequent expression of the Fushi tarazu protein, and in the expression of the 22C10 antigen shortly before the MP2 division. lethal of scute, atonal and asense, each not normally expressed in MP2, were tested for their ability to specifiy MP2 when ectopically expressed in the MP2 precursor. All proneural proteins are similarly able to promote the segregation of a neural precursor at the MP2 position but show distinct capabilities in its specification. achaete/scute mutants have CNS precursors in only 17% of the hemisegments, as determined with antibodies against Hunchback, a general neuroblast marker. A significant fraction of the remaining precursors do not express nuclear Prospero or Fushi tarazu, and none of the precursors express appreciable amounts of 22C10 antigen. Targeted expression of either achaete or scute is sufficient to sustain formation of normal MP2 precursors. Targeted expression of either l'sc, ase or ato promotes delamination of a neural precurosor at the MP2 position, however this putatitive MP2 precursor expresses FTZ only when its development is prompted by l'sc or ato; expression of 22C10 occurs only in the case of ato. Thus Ato seems to be an efficient replacement for Ac/Sc. Targeted Ato results in both progeny neurons projecting to the anterior, instead of the normal situation in which one progeny neuron projects to the anterior and the second projects to the posterior. Thus Ato causes the misspecification of the MP2 lineage. It is concluded that totally normal specification of the MP2 fate can only be attained by the proneural genes achaete or scute (Parras, 1996).
klumpfuss shows genetic interactions with achaete, scute, lethal of scute and asense. l'sc is able to activate klu expression, but apparently only in the wing disc. There appears to be only a weak influence of the AS-C genes on klu expression, restricted to the wing area of the wing disc. However, the overall expression pattern of klu is largely independent of proneural genes. The assumption that SOPs enter apoptosis in klu mutants is supported by the observation of abundant cell death in other developing organs of klu mutants, like the legs. At certain bristle positions, such as that of the anterior sternopleura, klu is required during early bristle development immediately after proneural gene function, in order to allow a particular epidermal cell to develop as a SOP. It is suggested that klu is required only for initiation of bristle development, being downregulated once specification takes place (Klein, 1997).
The magnitude of segregating variation for bristle number in Drosophila exceeds that
predicted from models of mutation-selection balance. To evaluate the hypothesis that
genotype-environment interaction (GEI) maintains variation for bristle number in nature,
the extent of GEI was quantitated for abdominal and sternopleural bristles among 98 recombinant inbred lines, derived
from two homozygous laboratory strains, in three temperature environments. There is considerable
GEI for both bristle traits. A genome-wide screen was conducted for quantitative trait loci (QTLs) affecting bristle number in each sex
and temperature environment, using a dense (3.2-cM) marker map of polymorphic insertion sites of roo
transposable elements. Nine sternopleural and 11 abdominal bristle number QTLs were detected.
Significant GEI is exhibited by 14 QTLs, but there was heterogeneity among QTLs in their
sensitivity to thermal and sexual environments. To further evaluate the hypothesis that GEI maintains
variation for bristle number, estimates of allelic effects across environments at genetic loci
affecting the traits are required. This level of resolution may be achievable for Drosophila bristle number because
candidate loci affecting bristle development often map to the same location as bristle number QTL, including achaete-scute, scabrous, hairy, and Delta (Gurganus, 1998).
In mutants lacking both the Achaete-Scute Complex (ASC) and atonal, coding for proteins known to establish SOP cell fate, two to three
neurons of the solo-MD type remain in the dorsal region of each abdominal hemisegment. The identity of these remaining neurons are
controlled by absent MD neurons and olfactory sensilla (amos). Both the ASC and Atonal physically interact with the protein Daughterless (Da).
Since the solo-MD neurons that exist in ASC;ato double mutants are eliminated in da mutants, this observation implies that the proneural gene for those solo-MD neurons also encodes a transcription factor of the bHLH family (Huang, 2000).
Amos is a novel bHLH protein and is expressed in
proneural clusters. This expression is later restricted to SOP cells. The technique of double-stranded RNA interference (RNAi), a procedure that mimics the effect of mutation, was used to eliminate amos function in embryos.
Loss of amos
function eliminates MD neurons that remain in ASC;atonal mutants. These results suggested that amos is required for the
formation of dbp and some dmd neurons, the neurons, which remain in ASC;ato double mutants. When misexpressed, amos induces the formation of all types of
sensory neurons. These results provide strong evidenct that
intrinsic differences among the proneural genes, specifically genes of the ASC, atonal and amos play a role in the induction of different types of sensory neurons (Huang, 2000).
In the embryonic ventral neuroectoderm of
Drosophila the proneural genes achaete, scute, and lethal of scute are expressed in clusters of
cells from which the neuroblasts delaminate in a stereotyped
orthogonal array. Analyses of the ventral neuroectoderm
before and during delamination of the first two
populations of neuroblasts show that cells in all regions
of proneural gene activity change their form prior to delamination.
Furthermore, the form changes in the neuroectodermal
cells of embryos lacking the achaete-scute
complex, of embryos mutant for the neurogenic gene
Delta, and of embryos overexpressing l'sc, suggest that
these genes are responsible for most of the morphological
alterations observed (Stollewerk, 2000).
Almost all neuroectodermal
cells are larger than the cells of the dorsal epidermal anlage (DEA). In comparison with the cells of the DEA in
early stage 8 embryos the dorsoectodermal cells of mid-stage
8 embryos are clearly smaller. A comparison
of the neurogenic region in early and mid-stage
8 embryos shows that the medial and intermediate regions
of the ventral neuroectoderm (VNE) do not increase further in size whereas
the lateral region enlarges considerably during this time.
Due to these morphological changes the VNE can now
be subdivided in relation to the cell sizes into three longitudinal
regions on both sides of the midline: medial,
intermediate, and lateral regions. In contrast to the cells
of the medial and lateral regions, which now have approximately
the same average values, the intermediate
cells are smaller. Only 20% of all cells in the intermediate region are
larger than the average, whereas 63% of the medial and
64% of the lateral cells exceed the average value.
Most of the enlarged cells have a cuboidal shape. In every hemisegment the apical
surfaces of two to four cells in the medial and lateral
regions are very small (12-16 µm2) but
expand basally to cover an area of 65-80 µm2. One or
two cells of this shape are also located in the intermediate
regions but are smaller basally (48-58 µm2) than the
medial and lateral cells. The number and position of
these cells suggest that they correspond to the delaminating
neuroblasts; this was confirmed by staining the embryos
with anti-Hunchback antibody, an early marker for neuroblasts (Stollewerk, 2000).
During delamination of the SI neuroblasts the neuroectodermal
cells gradually decrease in size, with the exception
of a few cells located close to the midline.
The cells that remain enlarged are either elongated
perpendicularly to the midline or have a rounded appearance.
Basally, between neuroectoderm and mesoderm,
large round cells are located that lose contact with the
apical surface at about 60% EL. On the basis of their position
and arrangement, as well as the analysis of embryos
stained for Hunchback, these cells can be identified as the SI neuroblasts.
Before delamination of the SII neuroblasts, cells in the
intermediate region of the neuroectoderm increase in
size. Most of the SII neuroblasts delaminate
from this region, whereas only a few neuroblasts arise
from the medial region, where enlarged cells can also be
detected. After delamination of the SII neuroblasts the enlarged cells shrink once again, as revealed by double staining with anti-Hunchback antibody
and phalloidin. Cells in all regions of the
VNE increase in size again prior to delamination of the
SIII neuroblasts. Thus, the VNE of wild-type embryos becomes morphologically
distinguishable from the DEA shortly before delamination
of the SI neuroblasts. At this point the cells of the
DEA have already divided, and about two-thirds of all cells in
the medial and the lateral regions have become enlarged
so that the DEA and the VNE are clearly distinguishable
due to differences in cell size. In addition, almost all cells
of the intermediate region increase in size prior to delamination
of the SII neuroblasts. These data are at odds with claims that only the neuroblasts enlarge prior to delamination, both in grasshopper and Drosophila (Stollewerk, 2000).
Is there a correlation between the activity of the ASC genes and the observed
morphological changes? The results presented indicate
that the ASC genes are not the only ones responsible
for the morphological changes that occur before
delamination of the SI neuroblasts. Although the number
of enlarged cells corresponds closely to the number of
cells that express the ASC genes at this time point, the
lack of the ASC does not result in all cells remaining the
same size. Whereas in the medial region of the VNE of
Df (1)260-1 embryos (that is, those lacking the ASC) only about 50% of the cells are
smaller in size than in the wild type, and the lateral region is
most strongly affected in comparison to the medial and
intermediate regions. Therefore the enlargement
of the neuroectodermal cells depends to a varying
degree on the activity of the ASC genes and is additionally
influenced by other factors. However, a clear correlation can be seen prior to delamination of the SII neuroblasts. At this time almost all
cells of the intermediate region increase in size, which
coincides with the expression of l'sc in this region. Furthermore, analysis of
the VNE of embryos lacking the ASC reveals that the
intermediate cells do not become enlarged prior to delamination
of the SII neuroblasts, suggesting that the observed
morphological changes are due to the activity of
the ASC genes at this point. In addition, the shrinkage of
the cells that had enlarged during delamination of the SI
and SII neuroblasts is correlated with the decrease in
ASC gene expression in the VNE at these time points (Stollewerk, 2000).
Analysis of wild-type and Delta mutant embryos also
suggests that the ASC genes are important for the maintenance
of the morphology of the neuroectodermal cells. Despite the fact that the total area of the intermediate region does not change significantly between early and
mid-stage 8, cell size changes can be detected in this region
shortly before delamination of the SI neuroblasts.
While 20% of the intermediate cells remain larger than
the average, the cells that had an average cell size in
the VNE of early stage 8 embryos now split into groups
of smaller cells. The fact that the number of cells that remain
larger than the average corresponds to the number
of cells that express the ASC genes in the intermediate
region suggests that the proneural genes are required to
keep these cells enlarged. This view is confirmed by analyses
of the VNE of Delta mutant embryos. In Delta mutant
embryos all cells of a proneural cluster continue to express the proneural genes and become neuroblasts. This altered gene expression causes all cells of a proneural cluster to remain enlarged until proneural gene expression is turned off (Stollewerk, 2000).
A correlation between increase in cell size and ASC
gene expression has also been shown by the analysis of
embryos labeled for ac protein and embryos overexpressing
l'sc. Area measurements reveal that 85% of
all cells that express ac are enlarged in these embryos.
The fact that not all ac-expressing cells are larger than
the average at the time point analyzed may be due to the
rapidity of the morphological changes (enlargement and
shrinkage) that occur immediately before and during
delamination of the neuroblasts. A clear influence of a
proneural gene on the cell sizes in the VNE can be seen
in embryos overexpressing l'sc: 45% more cells become
enlarged in the intermediate region in comparison to the
wild type. Only a minor increase in the numbers of enlarged
cells can be seen in the medial and lateral regions,
because two-thirds of these cells already express proneural
genes. In addition, the high proneural gene activity in
the VNE of embryos overexpressing l'sc causes the future
neuroblasts to change their morphologies: they expand
not only their basal but also their apical surfaces.
These data clearly show that the ASC genes have an influence
on the morphologies of the neuroectodermal cells (Stollewerk, 2000).
The achaete-scute complex of Drosophila has been the focus of extensive genetic and developmental analysis. Of the four genes at this locus, achaete and scute appear to act redundantly to specify the peripheral nervous system. They share cis-regulatory elements and are co-expressed at the same locations. A mutation removing scute activity has been previously described; it causes a loss of some sensory bristles. Thus, when Scute is absent, the activity of achaete allows formation of the remaining bristles. However, all existing achaete mutants are rearrangements affecting regulatory sequences common to both achaete and scute. To determine the level of redundancy between the two genes, a P element approach was used to generate a null allele of achaete, which leaves scute and all cis-regulatory elements intact. The peripheral nervous system of achaete null mutant larvae and imagos lacks any detectable phenotype. However, when the levels of Scute are limiting, then some sensory organs are missing in achaete mutant flies. achaete and scute are thought to have arisen from a duplication event about 100 Myr ago. The difference between achaete and scute null flies is surprising and raises the question of the retention of both genes during the course of
evolution (Marcellini, 2005; full text of article).
Home page: The Interactive Fly © 1995, 1996 Thomas B. Brody, Ph.D.
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achaete:
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