High impact information on pnr

• Sequencing studies show that, unlike most other transcribed repeats, the GATA repeats potentially contain open reading frames [1].
• This consists of repeats of the tetranucleotide GATA that are concentrated in the sex-determining region of the Y chromosome of mouse, on the W chromosome of snakes, and in the proximal region of the X chromosome of D. melanogaster, and it appears to be transcribed in a sex-specific and developmentally regulated manner [1].
• In contrast, the mutant pnr protein with lesions in this finger associates only poorly with Ush and activates transcription even when cotransfected with Ush [2].
• The distribution of REL and GATA sites within these DNAs suggests that most or all fat-specific immunity genes contain a common organization of regulatory elements: closely linked REL and GATA binding sites positioned in the same orientation and located near the transcription start site [3].
• Interactions between chip and the achaete/scute-daughterless heterodimers are required for pannier-driven proneural patterning [4].

Biological context of pnr

• Genetic interactions between dominant pnr mutants bearing lesions situated in the amino-terminal zinc finger of the GATA domain and ush mutants have been described [2].
• Our evidence suggests that during embryogenesis pnr activity is not essential for eye development [5].
• We argue that pnr acts like a classical selector gene but differs in that its expression is not propagated through cell divisions [6].
• The regulation of antimicrobial genes in larval fat depends on linked Rel/NF-kappaB and GATA binding sites [7].
• Multitype zinc-finger proteins of the Friend of GATA/U-shaped (Ush) class function as transcriptional regulators of gene expression through their modulation of GATA factor activity [8].

Anatomical context of pnr

• In support, we find that manipulation of pannier activity in either germ layer affects cardiac specification, suggesting that its function is required in both the mesoderm and the ectoderm [9].
• Serpent functions as the major GATA transcription factor in the larval fat body [7].
• Moreover, a dominant inhibitory GATA-binding fusion protein abrogates endoderm differentiation in intact embryos [10].
• We show that the GATA gene pannier is expressed in the dorsal mesoderm and required for cardial cell formation while repressing a pericardial cell fate [11].
• The GATA transcription factors are a family of C4 zinc finger-motif DNA-binding proteins that play defined roles in hematopoiesis as well as presumptive roles in other tissues where they are expressed (e.g., testis, neuronal and placental trophoblast cells) during vertebrate development [12].

Physical interactions of pnr

• Transcriptional activity of pannier is regulated negatively by heterodimerization of the GATA DNA-binding domain with a cofactor encoded by the u-shaped gene of Drosophila [2].

Regulatory relationships of pnr

• We show that L/Ser are expressed in entire early eye disc before the expression of pnr and Iro-C is initiated in late first instar dorsal eye margin cells [5].
• Moreover, Isl is coexpressed with Pnr in the posterior region of the mesothorax [13].

Other interactions of pnr

• We demonstrate that dorsal eye disc cells also become L or Ser dependent when they are ventralized by removal of pnr or Iro-C gene function [5].
• Recent studies suggest that ventral is the default state of the early eye, which depends on Lobe (L) function, and that the dorsal fate is established later by the expression of the dorsal selector gene pannier (pnr) [14].
• At a later stage, wingless expression expands ventrally from the pannier expression domain by a Wingless signaling-dependent mechanism [15].
• Interestingly, expression of pannier and u-shaped is regulated by Decapentaplegic signaling that provides the positional information along the anterior/posterior axis, in a concentration-dependent manner [15].
• We argue that eyg is a subordinate gene of the Iro genes, and that pnr mediates their thoracic patterning function [16].

Analytical, diagnostic and therapeutic context of pnr

• Site-directed mutagenesis of this element shows that these Tinman sites are critical to dSUR expression, and further genetic manipulations suggest that the GATA transcription factor Pannier is synergistically involved in cardiac-restricted dSUR expression in vivo [17].
• Significantly, direct binding for the C/EBP and GATA families of transcription factors was demonstrated in vitro by electrophoretic mobility shift assays (EMSA) [18].
• GATA: a graphic alignment tool for comparative sequence analysis [19].
• Chromatin Immunoprecipitation analysis revealed that both transcription factors were occupying the E2 box/GATA site in vivo [20].

References