ph, Polyhomeotic, DROZFP, EG:BACN25G24.3 , PHD
Gene model reviewed during 5.52
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.56
None of the polypeptides share 100% sequence identity.
1411 (aa); 135 (kD observed); 149 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ph-d using the Feature Mapper tool.
ph-d transcripts are present in 0-1.5hr embryos where they are significantly more abundant than ph-p transcripts. Levels drop off sharply and rise again in 3-6hr embryos. Levels drop off again after the 9-12hr embryo stage and remain low for all subsequent stages tested. Probes specific for ph-d and ph-p were used for the analysis.
ph transcripts are observed in the germarium and in stage 1-10 egg chambers. In later stages, staining is confined to nurse cells and follicle cells and is not seen in the ooctye. A light diffuse staining is observed in unfertilized eggs and early embryos. During the blastoderm stage, staining is observed in three stripes in the anterior of the embryo that extend from about 80% to 50% egg length. During gastrulation, expression is ubiquitous but is more intense in the ectoderm. During germ band extension, expression is more intense in parts of each parasegment and in germ band retraction, staining is more intense in CNS precursors. ph transcripts are observed in eye-antennal, leg, wing, and haltere discs in third instar larvae. While staining is observed all over the discs, some regions stain more intensely. For example, in eye-antennal discs, regions that will give rise to the posterior part of the eye and the orbital region as well as the proximal part of the antenna on the lateral side stain more intensely. The haltere disc consistantly shows a gradient of expression. The probes used do not distinguish between ph-p and ph-d transcripts.
ph protein starts to be detected in embryos in the nuclei at the periphery starting at cell cyle 10 and is clearly observed by cell cycle 11. In the cellular blastoderm stage, it is ubiquitously distributed but is more concentrated at the periphery and in central nuclei. Protein continues to be ubiquitously distributed in the embryo with higher concentrations in certain tissues. From gastrulation on, nuclei of cells that are undergoing mitosis appear to be more heavily stained. Within these putative mitotic domains, individual chromosomes appear to be stained. In stages 10 and 11, expression is periodic in the developing CNS. It is not clear if ph protein is in neuroblasts at stage 11 but it is present in neuroblast derivatives in stage 12 in the neuromeres of all segments. Expression in the nervous system continues throughout embryogenesis. ph protein is found mainly in the cell bodies of CNS neurons and may be present in glial cells. It is observed in the campaniform sensillae of the PNS in late embryos. ph protein is observed in eye-antennal, leg, wing, and haltere discs in third instar larvae. While staining is observed all over the discs, some regions stain more intensely. For example, in eye-antennal discs, regions that will give rise to the posterior part of the eye and the orbital region as well as the proximal part of the antenna on the lateral side stain more intensely. The haltere disc consistantly shows a gradient of expression. The antibody does not distinguish between ph-p protein and ph-d protein.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ph-d in GBrowse 2
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.
Source for identity of: ph-d CG3895
Pc, Scm, Psc, ph-p and ph-d contribute to the PRC1 (Polycomb repressive complex 1). PRC1 directly antagonizes ATP-dependent remodeling of nucleosomal arrays in a purified system and may directly modulate (and be modified by) SWI/SNF (brm/mor) activity.
The C-terminal region of ph-d can self-associate in vitro and this self-association is a function of the SAM domain.
Psc protein coimmunoprecipitates Pc and ph-d/ph-p indicating they are members of a common multimeric protein complex. These proteins are associated with identical regulatory elements of en in tissue culture cells and differentially distributed on regulatory sequences of inv.
In an effort to subdivide the Pc-group genes functionally, the phenotypes of adult flies heterozygous for every pairwise combination of Pc-group mutation were examined. Most duplications of Pc-group genes neither exhibit anterior transformations nor suppress the extra sex comb phenotype of Pc-group mutations, suggesting that not all Pc-group genes behave as predicted by the mass action model.
The bithorax complex genes are regulated by the Pc group of genes, including ph-p and ph-d, acting via 'Pc group response elements' (PREs), that can work even when removed from the normal bithorax complex context. The Pc group products apparently provide stable memory or imprinting of boundaries which are specified by gap and pair-rule regulators.
A member of the Polycomb group of genes; seems to be the strongly required both maternally and zygotically for normal embryonic development.
Two mutagenic events are necessary to produce null mutations, in both ph-d and ph-p. Single-event mutations are viable as males and homozygous females; such mutations produce transformations similar to those of known dominant gain-of-function mutants in the ANTC and BXC, i.e., transformation of wings to halteres, second and third legs to first legs and anterior abdominal segments to more posterior segments (mutants may also show loss of the humerus). Trans heterozygotes between viable and lethal alleles or between viable alleles and a deficiency for ph-d and ph-p die in late embryogenesis and exhibit posteriorly directed transformations; i.e. viable alleles are haplo-insufficient. The ph-d+/ph-p+ product is required autonomously in imaginal cells. A total lack of ph-d+/ph-p+ function prevents viability of the cuticular derivatives of these cells, but amorphic clones induced in late third instar survive.
The Pc group genes are negative regulators of homeotic genes and have pleiotropic effects on development.
At the shortened germ band stage (but not at the blastoderm stage), ph-d/ph-p seems to be involved in the regulation, not only of the homeotic genes Scr and Ubx, but also in the regulation of the segmentation genes ftz, eve and en.
Two-event lethal mutations die in mid-embryogenesis and completely lack ventral and abdominal epidermal derivatives; they show transformations of most of the segments toward the eighth abdominal segment. ph-d/ph-p has a strong maternal effect on segmental identity and epidermal development that cannot be rescued by a single paternally supplied dose of ph-d+/ph-p+ in the zygote.
There is an alteration in the pattern of axon pathways in the CNS in ph-d,ph-p mutants. The axons fail to form commissures or connectives but instead form large bundles in the middle of each hemi-ganglion.