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FB2026_01
,
released March 12, 2026
l'sc, T3, AS-C T3, lsc, EG:198A6.2
transcription factor - basic HLH - proneural gene that is also involved in specification of muscle progenitors
Please see the JBrowse view of Dmel\l(1)sc for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.51
Gene model reviewed during 5.55
There is only one protein coding transcript and one polypeptide associated with this gene
257 (aa)
258 (aa); 29 (kD)
Efficient DNA binding requires dimerization with another bHLH protein.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\l(1)sc using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as procephalic ectoderm anlage
Comment: reported as ventral nerve cord anlage
Comment: rows A, B, E, F
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
l(1)sc is expressed in posterior midline glia but not in anterior midline glia in stage 12 embryos.
At cellular blastoderm, l(1)sc transcripts are expressed in 12 dorsolateral stripes of alternating intensity which are interrupted by a narrow lateral nonexpressing strip and dorsal and ventral nonexpressing regions. At gastrulation, the weaker stripes increase in intensity. At germ band extension, the pattern of expression evolves into a "circle" pattern and subsequently into the "double stripe" pattern. The mRNA level appears constant throughout.
l(1)sc transcripts are uniformly distributed in early embryos. In the cellular blastoderm, transcripts are localized within stripes in the presumptive neurectoderm. By early gastrula, there is one stripe per metameric unit and transcripts are also detected in the procephalic neurogenic region. Between stages 8 and 9, the pattern changes to two stripes per metamere. l(1)sc is expressed in the segregating neuroblasts as well as in the cells that remain ectodermal. l(1)sc transcripts are also observed in cephalic neuroblasts and in the posterior midgut. In stages 11 and 12, l(1)sc is expressed by some ganglion mother cells. It then appears to be expressed in PNS precursors. Later expression appears to be restricted to the stomatogastric nervous system and the optic lobes.
l(1)sc transcripts are detected in a dynamic pattern from syncytial blastoderm through stage 11 embryos and are expressed in most neurogenic regions. In blastoderm embryos, l(1)sc is expressed in pairs of longitudinal bands located ventro- and dorso-laterally. Later, expression is seen in clusters of cells over most of the ectoderm. After stage 10 some clusters of expressing cells are found internally near the mesoderm. Expression is also seen along the midline and cephalic regions.
Comment: medial edge of the neurepithelium
l(1)sc-protein is expressed in cells of the larval outer optic anlage and in cells of the proximal part of the inner proliferation center that migrate towards the distal part.
l(1)sc is expressed in all midline precursors including MP1, MP3, MP4, MP5, and MP6 at embryonic stages 10-11 and in the MNB at stages 10-12. It remains present in the newly divided neurons of MP3 (H cell and H cell sib), MP5, and MP6. Levels persist in the H-cell longer than in H-cell sib. l(1)sc is undetectable in the progeny of MP1 and MP4. By the end of stage 11, it is no longer detectable in midline neurons. l(1)sc is present in PMG from stages 10-12 and occasionally appears weakly in 2 AMG.
l(1)sc is expressed in one or two rows of neural progenitor cells in the medial neurepithelial region in the developing optic lobe.
l(1)sc is transiently expressed in a narrow band of 1-2 cells at the medial edge of the neuroepithelial sheet. The band precedes neuroblast formation and moves laterally across the optic lobe throughout the third larval instar period. The l(1)sc-expressing cells lead a front that sweeps across the optic lobe (called a proneural wave) and induces neurepithelial cells to become neuroblasts.
Expression in procephalic neuroblasts stage 9-11: tritocerebrum - d1-d4, d6, d7, v3; deuterocerebrum - d1, d3, d6, d7, v2, v4-v6, v8; protocerebrum - ad1, ad3, ad5, ad7-10, ad13-15, ad17, av1, cd2, cd3, cd5, cd6, cd8-10, cd14-17, cd19-21, cv1-9, pd3, pd5, pd8-11, pd13, pd15, pd17, pd18, pv1-3
In stages 8-11 ac and l(1)sc proteins are expressed in a dynamic pattern in the procephalic neurectoderm in a largely complementary pattern. By stage 8 l(1)sc protein is detected in a large central domain and as development proceeds the area of protein expression increases. The first proto and deuterocerebral neuroblasts develop from this area. About 60% of all neuroblasts formed until stage 11 express l(1)sc. In stage 8 ac expression is detected in a small dorsal ocular and antennal group of cells. In stage 9 ac expression expands to several large domains in the neuroectoderm.
l(1)sc is expressed in a characteristic pattern in the mesoderm starting at embryonic stage 10. Between stage 10 and 12, it is expressed in at least 19 clusters of cells in each segment with some segment specificity to the pattern. In each cluster, one cell comes to express l(1)sc while expression is lost from other cells of the cluster. One or two cells from each cluster coexpress slou and l(1)sc. The progenitors divide and produce two cells that continue to express slou but not l(1)sc and are the founders of distinct muscles.
Significant l(1)sc protein accumulation begins well after RNA accumulation, from mid-stage 8 onwards. At the onset of the first wave of neuroblast segregation, only a subset of cells that express RNA also express protein. These l(1)sc protein-expressing cells are thought to be the segregating neuroblasts. In N and Dl mutants, l(1)sc protein expression is not limited to the neuroblasts, but occurs in all cells that accumulate RNA.
JBrowse - Visual display of RNA-Seq signals
View Dmel\l(1)sc in JBrowse
1-0
1-0.0
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.
Analysis of the function of l(1)sc.
The bHLH domains of the gene products encoded by the E(spl)-C and AS-C differ in their ability to form homo- and/or heterodimers. The interactions established through the bHLH link the products of the two complexes in a single interaction network which may function to ensure that a given cell retains the capacity to choose between epidermoblast and neuroblast fates until the cell becomes definitively determined.
All proneural proteins are similarly able to promote the segregation of a neural precursor at the MP2 neuroblast position but show distinct capacities in its specification.
The expression pattern of proneural genes of the AS-C and neurogenic genes of the E(spl)-C are examined in the procephlon and a map of the cells is constructed.
Loss of function and over-expression phenotypes indicate a role for l(1)sc in the segregation of muscle progenitors and the formation of the muscle pattern.
Overexpression of da using the GAL4 system, but not the ectopic expression of the AS-C genes l(1)sc or sc, leads to the formation of ectopic neural cells in embryonic tissue without neural competence. This effect os strongly enhanced by coexpressing l(1)sc or sc. Expression of da and/or l(1)sc is not sufficient to overcome the lateral inhibition in the analgen of the embryonic nervous system.
Ectopic expression does not affect the viability of either sex, but it does rescue the female lethality caused by ectopic expression of h.
Proneural gene products (ac, da and l(1)sc) activate transcription of Dl in the neuroectoderm by binding to specific sites within its promoter. This transcriptional activation enhances lateral inhibition and helps ensure that cells in the vicinity of prospective neuroblasts will themselves become epidermoblasts.
The l(1)sc gene has been cloned. A cluster of E boxes, upstream of the transcribed region, suggest regulation by helix-loop-helix gene products.
Ectopic expression shows that l(1)sc displays weak but significant feminizing activity.
Analysis of deficiencies revealed that l(1)sc affects the level but not the spatial pattern of ac expression.
In vitro DNA binding assays using gel retardation to an ac promoter region and hb zygotic promoter region target sequence demonstrates that da protein elicits a weak homodimeric binding and da/ac or da/sc heterodimers bind tightly. Single copy yeast promoters under the control of the GAL4 promoter were used to test whether ac, sc and da proteins could activate transcription of a Ecol\lacZ reporter gene in the yeast assay system, the l(1)sc gene does not induce Ecol\lacZ activity. Results suggest that da/l(1)sc heterodimers can function as transcriptional activators in direct proportion to their DNA-binding affinities.
The expression of l(1)sc protein before and during neuroblast segregation in the embryo has been studied.
DNA sequence analysis reveals four E box binding sites, for the binding of hetero-oligomeric complexes composed of da or AS-C proteins, in the first 877 bp of the ac upstream region. Electrophoretic mobility shift assays demonstrate that the emc protein can specifically antagonise DNA binding of the da/AS-C complexes in vitro in a dose-dependent manner, h and E(spl) proteins fail to exhibit this inhibitory effect.
A comparison of RNA and protein patterns suggests post-transcriptional regulation of l(1)sc. Protein accumulates in only a subset of the cells that express the RNA and these go on to become neuroblasts. The deployment of l(1)sc protein expression is one of the causal factors that assigns specific fates to the neuroblasts and a basis for the mechanism of lateral inhibition.
Ectopic expression of l(1)sc has no effect on sex determination.
Wild-type embryos show the protein is present in the developing neuroblasts, whereas the corresponding RNA is found in the neural and epidermal lineages. A study of the protein product distribution in mutants and wild type demonstrated that mutants cause neural hyperplasia in embryos.
The patterns of expression of ac, sc and l(1)sc are complex and evolve rapidly, affecting most if not all the known neurogenic regions. Gene expression precedes and is concomitant with the histological appearance of precursors of neural cells. The achaete-scute complex plays a role in determination and early differentiation of embryonic neural cells.
Deficiencies for most regions of the achaete-scute complex are hemizygous and homozygous viable; however, deficiency for l(1)sc is lethal.
Inferred from the inviability of In(1)sc4Lsc9R <up>left break of In(1)sc9 in doubt</up>, except in the presence of Dp(1;2)sc19. No mutant recovered (Garcia-Bellido, 1979).
Deficiency from which existence of l(1)sc inferred, i.e., In(1)sc4Lsc9R, embryonic lethal. Volume of embryonic ventral nerve cord slightly reduced; posterior commissures thinner than in wild type; longitudinal connectives virtually lacking. Concomitant deletions for scα or scα and ac cause more severe CNS disruptions, although by themselves these deletions have no observable CNS effects; simultaneous deletion of the scγ region also enchances the CNS disruptions (Jimenez and Campos-Ortega, 1987). Transiently expressed at periphery of syncytial blastoderm; late blastoderm shows paired dorsolateral and ventrolateral longitudinal stripes of expression, the latter being coincident with the presumptive neurogenic ectoderm. During germ-band expression, l(1)sc expression seen in many cell clusters over most of the ectoderm; segmental distribution becomes apparent both internally and externally. l(1)sc expression seen in many foci in the head region and in the posterior midgut rudiment (Romani, Campuzano and Modolell, 1987; Cabrera, Martinez-Arias and Bate, 1987). Little if any expression in later stages, except in the central nervous system (Romani, Campuzano, Macagno and Modolell, 1989).
Source for identity of: l(1)sc CG3839
