Jumeaux/Domina

DEVELOPMENTAL BIOLOGY

Embryonic

See the embryonic expression pattern of jumu at the Berkeley Drosophila Genome Project Patterns of Gene Expression Site.

Domina/Jumeaux is expressed in neural progenitors including NB4-2 and GMC4-2a. Antiserum was raised against a Jumu fusion protein. This polyclonal antibody (anti-Jumu) specifically recognizes the Jumu protein as evidenced by the fact that it fails to stain mutant embryos (e.g. jumu ^L70 homozygotes); in addition, the general embryonic staining pattern of anti-Jumu appears to parallel the expression pattern of the lacZ reporter gene in P1683. Consistent with its homology to the winged-helix family of transcription factors, Jumu protein shows nuclear localisation. Protein expression is first detected in the nuclei of syncitial embryos, indicating maternal expression, and appears to be present in all nuclei during cellular blastoderm. During germ band extension, and in the germ band extended embryo, nuclear expression is seen throughout the ectoderm and in the CNS primordia. During germ band retraction the ectodermal expression fades and Jumu expression is seen predominantly in the brain lobes, in the segmented CNS and elements of the PNS. The CNS expression persists into late embryogenesis. The NB expression pattern of Jumu is highly dynamic. To elucidate how jumu might act to generate the duplicated RP2 neurons, the expression of Jumu protein within the NB4-2 lineage was assessed. Pros is expressed in the nuclei of many GMCs in the developing CNS, including GMC4-2a, and can be used as a general GMC marker. At stage 10 (following SIII NB segregation), anti-Pros staining shows that there is a Pros + cell dorsal to NB4-2, indicating that the first round of NB4-2 cell division is complete and GMC4-2a is formed at this stage; the NB seen at the NB4-2 position at this time is NB4-2a; anti-Jumu and anti-Pros double-labellings indicate that NB4-2a is Jumu + at a time when GMC4-2a is not yet expressing Jumu protein; however, no Jumu + NB4-2 are seen prior to the formation of the Pros + GMC4-2a; therefore, Jumu is expressed in NB4-2 only after its first division. Later, during mid-stage 11, GMC4-2a expresses Eve just prior to its division (note that unlike Pros which is present in GMC4-2a when it is born, Eve expression commences only late in the GMC4-2a cell cycle); double labelling experiments with anti-Eve and anti-Jumu demonstrate that GMC4-2a also expresses Jumu at this time. Late in stage 11, GMC4-2a divides to produce the Eve + postmitotic RP2 and RP2 sibling cell; double labelling experiments indicate that both of these cells are also positive for Jumu shortly after their births. However, Jumu protein does not persist for long in the postmitotic neurons and can no longer be detected by the beginning of stage 12. These data indicate that within the NB4-2 lineage, Jumu accumulates only following the first NB cell division, in the nuclei of both NB4-2a and GMC4-2a. Jumu expression in NB4-2a precedes its expression in GMC4-2a (since a Jumu + GMC4-2a is never seen in conjunction with a Jumu - NB4-2a). Furthermore, Jumu protein is present in the nuclei of the postmitotic RP2 and its sibling (Cheah, 2000).

Hybridization of DIG-labeled probes shows ubiquitous distribution of Dom RNA in embryos of stages 1-4. In stages 5-6 Dom RNA amount is slightly reduced between 10% and 30% and is absent in pole cells. From stage 7, transcripts show very distinct concentration in cells of neurogenic regions, in cardial or pericardial cells, and possibly in gonad precursor cells -- this reflects the beta-galactosidase staining pattern of the enhancer trap strain. At the end of embryogenesis, Dom transcripts are found in the CNS, in maxillary cells, in gonad and imaginal disc precursor cells. In larvae, DIG-labeled Dom antisense RNA-probes and anti-Dom antibodies give strong signals in imaginal discs especially in neurogenic cells. In salivary glands, the strongest labeling is found in the ducts, in eye-antenna discs behind the morphogenic furrow and in developing ommatidia. The reduced fertility of homozygous Dom females and the high abundance of Dom RNA in early embryos as well as the lacZ expression in the enhancer trap line indicates maternal Dom expression. This is corroborated by the in situ hybridization of DIG-labeled RNA probes in ovaries. Dom RNA signals appear and increase in germ line cells of egg chambers from stages 1 to 9. Dom RNA is produced and stored in nurse cells until stage 10 when the RNA starts to be completely transferred to the oocyte (Strodicke, 2000).

Effects of Mutation

Homozygous mutants show rough eyes, irregular arrangement of bristles, extended wings, defective posterior wing margins, and a severely diminished vitality and fertility. Heterozygous Dom flies are morphologically wild type but show suppression of position-effect variegation. Consistently with this chromatin effect Dom protein is accumulated in the chromocenter and, as expected from a transcription factor, is found at specific euchromatic loci. Besides the suppression of PEV, the mutant morphological Dom phenotype, caused by all P-element alleles with exception of Dom^l(3)06142, involves aberrant structures of eyes and wings and a mutant arrangement of bristles. Rough eyes with only a few mechanosensory bristles is the most obvious feature of this phenotype. The eyes of homozygous mutant Dom fiies are smaller than wild-type eyes; adjacent ommatidia are often fused and the eyes are composed of ommatidia of variable size and shape This is probably due to the incompletely formed mesh of pigment cells that usually shapes ommatidia into a regular hexagonal structure. In histological tangential sections of wild-type eyes, seven round rhabdomeres are observed in a regular array whereas the outer irregular facet array observed in homozygous Dom mutants corresponds to an inaccurate underlying cell pattern. Sections from homozygous Dom^D631 eyes reveal a variable number of rhabdomeres with distorted shapes in unusual positions in the ommatidia The mutant bristle phenotype suggests that Dom is involved in adult PNS development. In most cases homozygous mutant Dom flies show loss or doubling of macrochaetae, however, bristles appear at correct positions. This indicates that extra bristles arise from the normal complement of proneural clusters. They have sockets and shafts and, therefore, obviously represent complete sensory organs (Strodicke, 2000).

The wings are weakly affected by Dom mutations. Wing size is reduced, hairs are irregularly arranged, posterior wing margins are notched and L5 is sometimes shortened. In some cases wings are extended. The mutant Dom phenotype is caused by the P[lArB] integration D631 while the wild-type phenotype is restored in excision lines after remobilization of the P[lArB] transposon. In accordance with the mutant phenotype, lacZ expression of the P[lArB] transposon was found in all affected tissues. In late embryos and in first and second instar larvae, the beta-galactosidase staining suggests Dom expression mainly in the CNS. In larvae, the CNS, imaginal discs, gonadal anlagen, and salivary glands are stained. Strong lacZ expression is observed in eye discs behind the morphological furrow and in sensory and bristle precursor cells of wing and leg discs. In adults, lacZ is expressed in ovaries and in testes (Strodicke, 2000).

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date revised: 5 March 2005

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