Gene Dmel\Pcl

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General Information

Symbol

Dmel\Pcl

Species

D. melanogaster

Name

Polycomblike

Annotation symbol

CG5109

Feature type

protein_coding_gene

FlyBase ID

FBgn0003044

Created / Updated

2003-12-01/2003-12-01

Genomic Location

Chromosome (arm)

Recombination map

2-84

Cytogenetic map

55B8-55B8

Sequence location

2R:14,022,934..14,026,965 [+]

Map ( GBrowse )

Summary Information

Automatically generated summary

See sections below for more information

The gene Polycomblike is referred to in FlyBase by the symbol Pcl (CG5109, FBgn0003044). It has the cytological map location 55B8. Its sequence location is 2R:14022934..14026965. Its molecular function is described as: DNA binding; transcription factor activity; protein binding; zinc ion binding. It is involved in the biological processes: chromatin modification; negative regulation of transcription, DNA-dependent. 33 alleles are reported. The phenotypes of these alleles are annotated with 47 unique terms, many of which group under: adult segment; embryonic abdomen; larval abdominal segment; embryonic segment; adult; thoracic segment; embryonic tagma; abdominal segment 7; appendage segment; adult mesothoracic segment. It has one annotated transcript and one annotated polypeptide.

External Summaries

Phenotypic Description from the Red Book (Lindsley & Zimm 1992)

Gene/Allele symbols may differ from current usage

Pcl: Polycomblike

Pcl+, like Pc+, may be considered a negative regulator of the BXC and the ANTC. Strong Pcl mutant alleles (Pcl1, Pcl2) are homozygous lethal, hemizygous lethal, and lethal with each other, the embryos having partial posteriorly-directed transformations of the abdominal segments (segment 1 into segment 2 and segments 2-7 into more posterior segments). These mutants are strong enhancers of Pc3, showing Pc-like transformations in embryos, and are indistinguishable from Pcl deficiencies in complementation behavior. Extreme posteriorly-directed segmental transformations are found in Pcl1/Df(2R)Pcl11B;Pc3/Pc3 lethal embryos (Duncan, 1982); these embryos are considerably more abnormal than the Pc3 homozygotes that are Pcl+. Pcl/Pcl embryos that are also homozygous for Asx, Psc, or Scm show strong posteriorly-directed transformations of the entire body pattern; the triple mutant Psc Asx Pcl has a tandem array of posterior abdominal segments including four abdominal denticle bands in the head region (Jurgens, 1985). Pcl1/Pcl1 clones in the second through the sixth abdominal tergites also show caudal transformations; similar clones in the wing often appear to be partially transformed into haltere tissue. Weak Pcl alleles (Pcl3, Pcl4) survive, at least through eclosion, either as homozygotes or as heterozygotes with strong or weak Pcl alleles (Duncan, 1982). Pcl1/Pcl3 and Pcl1/Pcl4 show segmental transformations characteristic of Pc/+ flies, i.e. antenna to leg, second and third leg to first leg, wing to haltere, and posteriorly-directed abdominal transformations (the most frequent abnormality). Increasing the dosage of the BXC in Pcl1/Pcl4 heterozygotes suppresses the posteriorly-directed transformations, but enhances the transformations from leg2 and leg3 to leg1; increasing the dosage of the ANTC enhances both types of transformations (Duncan, 1982). Pcl1/Pcl3 females, which die before or soon after eclosion, show a conversion of parovaria to spermathecae. Both strong and weak Pcl alleles are viable as heterozygotes (Pcl/+) and may show partial abdominal and leg transformations, the abnormalities increasing in Pcl/+;Pc/+ flies or when Pcl/+ is combined with E(Pc).