Disease relevance of svp

• When reaching the next temporal identity, this expression is switched off in the neuroblasts by seven up (svp) in a mitosis-dependent manner, but is maintained in their progeny (ganglion mother cells) [1].

High impact information on svp

• Molecular analysis of svp reveals that it is a member of the steroid receptor gene superfamily and is likely to be a Drosophila homolog of the human transcription factor COUP [2].
• The Drosophila seven-up (svp) gene was isolated as a lethal insertion in an "enhancer trap" screen [2].
• We show that the COUP-TF-related nuclear orphan receptor Seven-up is a key component that becomes induced in response to mitogenic EGF receptor signaling activity emanating from the tip cell [3].
• Seven-up in turn is capable of regulating the transcription of cell cycle regulators [3].
• Seven-up, the Drosophila homolog of the COUP-TF orphan receptors, controls cell proliferation in the insect kidney [3].

Biological context of svp

• Recent results provided evidence that the dependency of Svp activity on mitosis could be due to an inhibition of the nuclear export of svp mRNA [4].
• Transition to Kr requires the termination of hb expression, which occurs in response to mitosis, and is mediated by Seven-up (Svp) [4].
• Moreover, strong psq alleles are dominant suppressors of a svp-induced cone cell transformation phenotype [5].
• Strikingly, although the complete downregulation of hb is mitosis dependent, the lineage-specific timing of svp upregulation is not [1].
• However, a decrease in ras signaling results in enhancement of the phenotype caused by the ro-svp transgene [6].

Anatomical context of svp

• Although the gene was previously identified and described as a member of the maternal posterior group of genes, the strong semilethal alleles isolated here demonstrate a specific requirement for psq function downstream of svp for the development of photoreceptors R3/R4 [5].
• Mapping and complementation testing with candidate mutations revealed new alleles of the neuronal fate determinant svp and the synaptic vesicle trafficking component lap among the collection of mutants recovered in this screen [7].
• Several members of the steroid receptor superfamily, including the transcription factor COUP, are closely related to the Drosophila gene seven-up (svp) which is required for the development of the embryonic central nervous system (CNS) and specific photoreceptor cells of the eye [8].
• Thus, svp plays a role in fat-body-specific expression of at least two terminal fat-cell differentiation genes [9].
• In contrast to svp, we found no evidence that the steroid receptor HNF-4(D) gene was expressed in the fat body nor that it was involved in the development of this tissue [9].

Associations of svp with chemical compounds

• A novel vertebrate svp-related nuclear receptor is expressed as a step gradient in developing rhombomeres and is affected by retinoic acid [10].

Regulatory relationships of svp

• In the non-Tin-expressing pairs of cardioblasts, tinc transcription seemed to be repressed by Seven-up [11].
• The pipsqueak (psq) gene is expressed at high levels in the R3/R4 precursors during eye development and this expression depends on seven-up (svp) gene function [5].
• In the ganglion mother cell, svp is repressed by Prospero, a transcription factor asymmetrically localised to this cell during mitosis [1].
• Seven-up inhibits ultraspiracle-based signaling pathways in vitro and in vivo [12].

Other interactions of svp

• Thus, the differential regulation of hb between the neuroblasts and the ganglion mother cells is achieved by a mechanism that integrates information created by the asymmetric distribution of a cell-fate determinant upon mitosis (Prospero) and a transcriptional repressor present in both cells (Seven-up) [1].
• Transient expression under the sevenless enhancer of either svp isoform leads to a dosage-dependent transformation of cone cells into R7 photoreceptors, and at a lower frequency, R7 cells into outer photoreceptors [13].
• We show that the transcription of seven up (svp), which is expressed in the two most posterior pairs of cardioblasts in each segment, is dependent on hedgehog (hh) signaling from the dorsal ectoderm [14].
• Since we find that mutations in the Egf-receptor are also among the strongest suppressors of svp-mediated cone cell transformation, we propose that the Ras activity in cone cells is due to low level Egfr signaling [13].
• With respect to their position and the expression of the markers asense (ase) and seven-up (svp), 23 small groups of one to five neuroblasts each were identified [15].

References