High impact information on aop

• Depolymerization of Yan by Mae represents a novel mechanism of transcriptional control that sensitizes Yan for regulation by receptor tyrosine kinases [1].
• This interaction is cooperative when both proteins are targeted to the same promoter and is antagonized by another ETS domain protein, YAN, a negative regulator of R7 development [2].
• This phosphorylation is both necessary and sufficient to abrogate transcriptional repression by Yan. Mae also regulates the activity of the transcriptional activator Pointed-P2 by a similar mechanism [3].
• Furthermore, we present genetic and biochemical data suggesting that MAP kinase controls neural development through phosphorylation of two antagonizing transcription factors of the ETS family, Yan and PntP2 [4].
• DJun and Aop regulate dpp expression in the most dorsal row of cells [5].

Biological context of aop

• These findings suggest that, prior to Ras activation, the Mae/Yan interaction blocks premature nuclear export of Yan monomers [6].
• After activation, transcriptional up-regulation of Mae apparently leads to complete depolymerization and export of Yan [6].
• In undifferentiated cells of the larval eye imaginal disc, the transcriptional repressor Yan outcompetes the transcriptional activator Pointed for ETS binding sites on the prosperoenhancer [7].
• Phosphorylation and downregulation of Yan is facilitated by a protein called Mae [1].
• Function of the ETS transcription factor Yan in border cell migration [8].

Anatomical context of aop

• pokkuri, a Drosophila gene encoding an E-26-specific (Ets) domain protein, prevents overproduction of the R7 photoreceptor [9].
• EGF receptor signaling induces pointed P1 transcription and inactivates Yan protein in the Drosophila embryonic ventral ectoderm [10].
• Previous work in cultured cells has led us to propose that MAE attenuates the transcriptional activity of both YAN and POINTED, although its effects on POINTED remain controversial [11].
• Ovarian follicle cells also contain Yan protein [12].

Physical interactions of aop

• Mae has been shown to bind the Yan and Pointed-P2 transcription factors, thereby changing their ability to activate or repress target genes [13].
• Biochemical and genetic analysis indicated that the minimum btl enhancer includes binding sites of Anterior-open [14].

Enzymatic interactions of aop

• Hyperstable Yan (ACT) cannot be phosphorylated and blocks prospero expression [7].

Regulatory relationships of aop

• Yan regulates Lozenge during Drosophila eye development [7].
• We find that Anterior Open must be inactivated for posterior Engrailed cells to adopt their correct fate [15].

Other interactions of aop

• In this way, Yan and Pointed are essential for prospero regulation [7].
• The simultaneous effects of the DER pathway on pntP1 induction and Yan inactivation may contribute to the definition of the border of the ventralmost cell fates [10].
• We demonstrate that the molecular mechanism underlying downregulation of YAN involves CRM1-mediated nuclear export and define a novel role in this context for MAE, a co-factor previously implicated in facilitating MAPK phosphorylation of YAN [16].
• Thus, we propose that MAE plays multiple independent roles in fine-tuning the levels of POINTED and YAN activity in accordance with changing RTK signaling conditions [16].
• Here, we show that Yan, an Ets transcriptional repressor that blocks cellular potential for specification and differentiation, is a target of Notch signaling during Drosophila eye development [17].

References