ph, Polyhomeotic, PHP, EG:87B1.5 , ph-proximal
Gene model reviewed during 5.52
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.56
6.4, 6.1 (northern blot)
Component of PRC1 complex, which contains many PcG proteins like Pc, ph, Scm, Psc, Sce and also chromatin-remodeling proteins such as histone deacetylases. This complex is distinct from the Esc/E(z) complex, at least composed of esc, E(z), Su(z)12, Rpd3 and Caf1-55. The 2 complexes however cooperate and interact together during the first 3 hours of development to establish PcG silencing. Interacts with the SAM domain of Scm via its SAM domain in vitro. Interacts with Trl in vivo and with corto in vitro.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ph-p using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ph-p 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.
Pc-G proteins can silence gene expression at a large number of chromosomal locations. Repression is observed even with separation distances of up to 3.0kb between target promoters and binding sites for tethered Pc-G proteins. Silencing depends upon the dosage of endogenous, untethered ph-d/ph-p protein, implying that tethered proteins work by recruiting other Pc-G components.
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-p can self-associate in vitro and this self-association is a function of the SAM domain. Mutational analysis identifies the residues important for oligomerisation.
ph-p, Psc and Pc proteins coimmunoprecipitate from nuclear extracts. Interacting domains are identified and delimited using the two-hybrid system, the interactions are shown to be direct by using an in vitro binding assay.
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.
Early ph-p gene expression is under the control of bcd and en as activators and of osk as an inhibitor. The negative autoregulation of ph-p starts at the blastoderm stage and is partly mediated by a transvection effect. As the number of functional copies of ph-p increases a concomitant reduction of the transcription in each copy is observed. This regulation is ensured positively by the trx group and negatively by the Pc group gene products. An equilibrium between these two states of chromatin activity ensures an accurate level of ph-p transcription.
P-element transposons bearing ph-p regulatory sequences preferentially insert into regions containing known ph-p and Pc protein binding sites, perhaps because shared regulatory proteins bring transposons and insertion sites into close proximity.
Sequences from the 5' region of ph-p confer variegation on mini-w and Ecol\lacZ genes in euchromatic contexts. This variegation is sensitive to ph-p and Pc mutations. The ph-p regulatory DNA can also mediate transvection of the mini-w gene, which is abolished in ph-p but not z mutant backgrounds.
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.
ph-p protein contains a possible zinc finger motif, a Ser/Thr-rich region and Gln repeats, consistent with a role for ph-p in DNA and protein interactions. ph-p protein binds to about 80 sites on polytene chromosomes and extensive overlap exists between the binding sites of ph-p and Pc on polytene chromosomes.
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.