High impact information on pnt

• We present evidence that JUN interacts with the ETS domain protein Pointed to promote R7 formation [1].
• The Drosophila gene pointed (pnt) encodes two putative transcription factors (P1 and P2) of the Ets family, which in the embryonic CNS are found exclusively in glial cells [2].
• Therefore, both the pnt loss-of-function as well as the gain-of-function phenotype suggest that glial cells are able to induce 22C10 expression on neighboring neurons [2].
• Loss of pnt function leads to poorly differentiated glial cells and a marked decrease in the expression of the neuronal antigen 22C10 in the MP2 neurons, which are known to interact intimately with the pntP1-expressing longitudinal glial cells [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].

Biological context of pnt

• However, EDL/MAE functions as an antagonist of Pointed P2, by binding to its Pointed domain and abolishing its transcriptional activation function [4].
• The constriction divides the abdA domain of the midgut into two chambers, the anterior one producing the Pointed (Pnt) ETS transcription factors and the posterior one the Odd-paired (Opa) zinc finger protein [5].
• Here we show that the ETS domain protein encoded by the P2 transcript of the pointed (pnt) gene is a nuclear target of this signalling cascade which acts downstream of Rl/MAP kinase [6].
• The gene pointed (pnt) is required for this glial-neuronal cell interaction, as loss of function mutations lead to a change in the migration behavior of the midline glial cells [7].
• The ETS domain protein pointed-P2 is a target of MAP kinase in the sevenless signal transduction pathway [6].

Anatomical context of pnt

• In different types of glial cells, REPO can act alone, or cooperate with either TTK69 or PNTP1 to regulate different target genes [8].
• EGF receptor signaling induces pointed P1 transcription and inactivates Yan protein in the Drosophila embryonic ventral ectoderm [9].
• As shown by pole cell transplantations, spi and S are also required for normal development of the female germ line, while sim, rho, and pnt appear to be exclusively zygotically expressed, and the maternal gene sic acts in the germ line autonomously [10].
• As ectopically expressed pointedP1 can also rescue pointedP2 deficiency in photoreceptor development, it appears that the ability of ets products to phenocopy each other in vivo does not require the conserved RII/pointed box, but rather, primarily relies on the presence of the highly conserved ETS domain [11].
• In the embryonic central nervous system pointedP2 is required for midline glial cell differentiation, whereas, in the eye, pointedP2 is essential for photoreceptor cell differentiation [11].

Associations of pnt with chemical compounds

• Threonine 82 is part of a sequence that is conserved in Drosophila Pointed P2, an ets protein that has been shown both genetically and biochemically to mediate Ras signalling in Drosophila cells [12].

Physical interactions of pnt

• Mae binding to Pnt-P2 occludes this docking surface, thereby acting to downregulate Pnt-P2 activity [13].

Regulatory relationships of pnt

• While expression of pointedP2 is induced by Wingless signalling, seven up is initiated in a subset of the PointedP2 cells through the activity of the proneural genes [14].
• In the midline glia pointedP2 in turn activates the transcription of argos, which encodes a diffusible negative regulator of EGF-receptor signalling [15].
• This suggests that Pointed normally down-regulates EGF receptor signaling in the midline to generate patterning in the dorsal region [16].

Other interactions of pnt

• The activity of at least one of these regulators, Pointed, is controlled by EGFR signalling [17].
• Here we show that two antagonistic transcriptional regulators, Pointed, an activator, and Tramtrack69, a repressor, directly regulate the transcription of string [17].
• This suggests that inducing cells, which can respond to Spitz they themselves produce, must somehow prevent activation of Pointed P2 [4].
• EDL/MAE regulates EGF-mediated induction by antagonizing Ets transcription factor Pointed [4].
• The members of the spitz group differ from one another: sim affects a more median strip of the ventral ectoderm than the other zygotic genes and pnt causes separation rather than deletion of pattern elements [10].

Analytical, diagnostic and therapeutic context of pnt

• We use site-directed mutagenesis and yeast two-hybrid analysis to show that conserved amino acids within the alternate Lozenge exon are important for interaction with Pointed [18].

References