PntP1, PntP2, D-ets-2, pointedP2, pointed-P1
transcription factor - ets family - a target of Egf signaling - required for the differentiation of glial cells in the ventral nerve cord - required downstream of Ras in the development of the eye prevents both premature differentiation and dedifferentiation of Drosophila intermediate neural progenitors
Please see the JBrowse view of Dmel\pnt for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.47
4.2, 4.0 (northern blot)
4.4 (northern blot)
4.7 (northern blot)
None of the polypeptides share 100% sequence identity.
718, 623 (aa); 78, 67 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\pnt using the Feature Mapper tool.
Comment: maternally deposited
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 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
Comment: reported as procephalon primordium
Comment: reported as procephalon primordium
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
Comment: reported as head epidermis primordium
Comment: reported as procephalon primordium
pnt mRNA is highly enriched in the lysate extracted from larval brains enriched with type II neuroblasts.
Transcript is expressed in the intermediate groups and R8 photoreceptor equivalence groups of the developing retina.
During induction of bract cells in pupae, pnt is initially upregulated in all cells adjacent to bristle lineage cells at 30h APF, but it is highest in the bract cell and is lost from other cells by 36h APF.
pnt expression is observed in Type II neuroblast lineages in third instar larvae.
pnt expression is observed in the Bolwig organ primordium from embryonic stage 10/11 to stage 12/13 and is gone by stage 15.
With an antibody that detects both pnt protein isoforms, pnt protein is detected in the nuclei of ommatidial precursor cells. In a background that is mutant for the 718 amino acid P2 isoform, most all nuclear staining is eliminated, except for clusters of nuclei in the morphogenetic furrow, and scattered nuclei in the posterior part of the eye. This staining presumably corresponds to the P1 isoform, and is in good agreement with the distribution of the P1 transcript.
With an antibody that detects both pnt protein isoforms, pnt protein is detected in the nuclei of ommatidial precursor cells. In a background that is mutant for the 718 amino acid P2 isoform, most all nuclear staining is eliminated, except for clusters of nuclei in the morphogenetic furrow, and scattered nuclei in the posterior part of the eye. This staining presumably corresponds to the P1 isoform, and is in good agreement with the distribution of the P1 transcript. In photoreceptor precursors, the appearance of pnt P2 protein precedes the appearance of elav protein, and after about 4-6 hours of co-expression, pnt P2 protein is no longer detected.
GBrowse - Visual display of RNA-Seq signals
View Dmel\pnt in GBrowse 2Please 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 GBrowse 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
The pnt-P1 isoform prevents both the premature differentiation and the de-differentiation of intermediate neural progenitors in the type II neuroblast lineage.
pnt is required cell-autonomously along the dorsal midline to repress dorsal appendage fate.
S2 cells treated with dsRNA generated against this gene show reduced phagocytosis of Candida albicans compared to untreated cells.
Seven EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
Candidate gene for quantitative trait (QTL) locus determining bristle number.
Identification: Enhancer trap expression pattern survey for loci expressed in the ring gland.
ttk is required for proper glial cell development in the CNS. Phenotypes of doubly mutant ttk and pnt embryos and ectopic expression of ttk and pnt indicates the existance of two independent genetic pathways regulating glial cell development, which in the lateral glia are both downstream of gcm. One, mediated via pnt, results in the activation of glia cell differentiation, whereas the other, mediated by ttk, results in the suppression of neuronal differentiation in these cells.
In vivo culture of mutant discs from genotypes that are normally embryonic lethal demonstrates pnt is required for wing disc growth.
The primary target genes of Egfr are pnt, vnd and Fas3, these are induced in different ectodermal domains. Secondary target genes oc, argos and trn are activated by pnt in response to Egfr signalling. The proper induction of these genes requires the concomitant inactivation of aop, mediated by Egfr signalling.
Inactivated mutations of Ras85D enhance the P{sevhs-cswCS} phenotype.
pnt is required in dorsal follicle cells for patterning of the cell layer into either appendage-producing or midline cells. Loss of pnt results in the loss of midline cells and an excess of appendage-forming cells, a phenotype associated with overactivation of the EGF receptor pathway in the dorsal region. Overexpression of pnt leads to a phenotype similar to that generated by loss of the EGF receptor pathway. Data indicates a novel antagonistic function for pnt in oogenesis: in response to activation of the EGF receptor pnt is expressed and negatively regulates the EGF receptor pathway, possibly by integrating information from a second pathway.
The pnt transcription factor is required for secondary branching and also to activate expression of terminal branch markers.
pnt is required for neuronal glial cell interactions: loss of function mutations lead to a change in the migration behavior of the midline glial cells.
Two different and distinct trans-acting DNA domains control the pnt P2 promoter activity, one is an activator, the other a repressor. Enhancers directing tissue specific pnt P2 expression are located 3' to the first P2 exon within intronic sequences. Heteroallelic complementation reveals that the pnt gene product is required during eye, wing and haltere development.
pnt has been cloned, sequenced and its RNA expression pattern characterised.
pnt gene product is required for the proper development of the ventralmost cuticle and the CNS midline.
Zygotically active locus involved in the terminal developmental program in the embryo.
pnt mutants display a pointed head skeleton and deletion of the medial portion in all denticle belts.