High impact information on vvl

• Moreover, misexpression of Acj6 in lPNs, or Drifter in adPNs, results in dendritic targeting to glomeruli normally reserved for the other PN lineage [1].
• Here we show that POU domain transcription factors, Acj6 and Drifter, are expressed in adPNs and lPNs respectively, and are required for their dendritic targeting [1].
• We find that the class III POU protein, Drifter (Ventral veinless), is co-expressed with Islet and Lim3 specifically in the ISNb motoneuron subclass [2].
• Characterization of the 'dorsal chordotonals' phenotype of vvl mutant embryos revealed that in the absence of VVL, cell fates within the lch5 lineage are determined properly and the entire organ is misplaced [3].
• In this process, VVL function is required in the ectoderm and possibly in the lch5 organs too [3].

Biological context of vvl

• Mutations in the u-turn (ut) locus perturb the localization of lch5 neurons and result in a 'dorsal chordotonals' phenotype [3].
• In the embryo, loss of VVL function results in increased apoptosis in specific es organs [3].
• Analysis of vvl mutant clones in adults revealed a requirement for VVL in the control of cell number within the bristle lineage [3].
• These results suggest that the Drifter protein, which maintains its own expression through a tracheal-specific autoregulatory enhancer, is not necessary for initiation of breathless expression but functions as a direct transcriptional regulator necessary for maintenance of breathless transcripts at high levels during tracheal cell migration [4].
• In addition, breathless regulatory DNA contains seven high affinity Drifter binding sites similar to previously identified Drifter recognition elements [4].

Anatomical context of vvl

• The Drosophila drifter (dfr) gene, previously referred to as Cf1a, encodes a POU-domain DNA-binding protein implicated as a neuron-specific regulator in the developing central nervous system (CNS) [5].

Physical interactions of vvl

• I-POU has been previously reported to inhibit DNA binding by the POU-III class factor drifter/Cf1a via the formation of heterodimeric complexes [6].

Regulatory relationships of vvl

• These results indicate that through activation of its target genes, vvl makes the tracheal cells competent to further signalling and suggest that the btl transduction pathway could collaborate with other transduction pathways also regulated by vvl to specify the tracheal branching pattern [7].

Other interactions of vvl

• By Northern analysis, all three of the genes are expressed in early embryos; the pdm-1 and Cf1a genes are also expressed at lower levels throughout development [8].
• The spatial expression patterns of the pdm-2 and Cf1a genes show that they probably play multiple roles during development: an early role in specific ectodermal cells, and a subsequent role in the embryonic nervous system [8].
• Our results demonstrate that Drifter functions along with MAD as a direct activator of Vestigial expression in the wing pouch [9].
• Morphogenesis of the tracheal tree requires the activity of many genes, among them breathless (btl) and ventral veinless (vvl) whose mutations abolish tracheal cell migration [7].
• Here we show that, in addition, vvl is independently required for the specific expression in the tracheal cells of thick veins (tkv) and rhomboid (rho), two genes whose mutations disrupt only particular branches of the tracheal system [7].

References