High impact information on SoxN

• Taken together, these data indicate that SOXB1 signaling is both necessary and sufficient to maintain panneural properties of neural progenitor cells [1].
• The phenotype elicited by inhibition of SOX2 signaling can be rescued by coexpression of SOX1, providing evidence for redundant SOXB1 function in CNS progenitors [1].
• Evidence for differential and redundant function of the Sox genes Dichaete and SoxN during CNS development in Drosophila [2].
• Genetic interactions of SoxNeuro and the dorsoventral patterning genes ventral nerve chord defective and intermediate neuroblasts defective underlie ventral and intermediate neuroblast formation [3].
• Formation of neuroblasts in the embryonic central nervous system of Drosophila melanogaster is controlled by SoxNeuro [3].

Biological context of SoxN

• By contrast, in the medial neuroectoderm, where the expression of SoxNeuro and Dichaete overlaps, the phenotypes of both single mutants are mild [2].
• The sequence in SoxNeuro targeted for SUMOylation, IKSE, is part of a small inhibitory domain, able to repress in cis the activity of two adjacent transcriptional activation domains [4].

Anatomical context of SoxN

• SoxN is expressed in a highly dynamic pattern during embyogenesis, being associated with the development of the central nervous system (CNS), from the early steps onwards [5].
• In this report, we show that SoxN expression persists in a subset of neurons and glial cells of the ventral nerve cord at embryonic stages 15/16 [6].
• We demonstrate that SoxNeuro is essential for the formation of the neural progenitor cells in central nervous system [3].

Regulatory relationships of SoxN

• In human cell culture assays, SoxN represses Tcf-responsive reporter expression, indicating that the fly gene product can interact with mammalian Wnt pathway components [7].

Other interactions of SoxN

• Through a yeast two-hybrid assay searching for proteins interacting with SoxN, we have isolated a novel protein in Drosophila, SoxNeuro Co-Factor (SNCF) [8].
• We identified several genes involved in the regulation of axon scaffolding as potential direct target genes of SoxN, including beat1a, semaphorin2a, fasciclin2, longitudinal lacking and tailup/islet [6].
• In accordance with an at least partially redundant function in that region, SoxNeuro/Dichaete double mutant embryos show a severe neural hypoplasia throughout the central nervous system, as well as a dramatic loss of achaete expressing proneural clusters and medially derived neuroblasts [2].

Analytical, diagnostic and therapeutic context of SoxN

• In an attempt to address SoxN function in late stages of CNS development, we have used a chromatin immunoprecipitation approach to isolate genomic regions bound in vivo by SoxN [6].

References