High impact information on knrl

• The consequence of this difference in intron size is that knrl cannot substitute for kni segmentation function, although it gains this ability when expressed from an intronless transgene [1].
• The Drosophila gene knirps-related is a member of the steroid-receptor gene superfamily [2].
• Finally, kni and knrl are likely to refine the L2 position by positively auto-regulating their own expression and by providing negative feedback to repress salm expression [3].
• The transcription factors KNIRPS and KNIRPS RELATED control cell migration and branch morphogenesis during Drosophila tracheal development [4].
• These studies support a model in which both the Dpp- and the FGF-signaling pathways control expression of knirps and knirps-related, thereby regulating cell migration during dorsal branch formation [5].

Biological context of knrl

• These experiments provide a mechanistic basis for understanding how kni and knrl link AP patterning to morphogenesis of the L2 vein by orchestrating the expression of a selective subset of vein-promoting genes in the L2 primordium [6].
• Identical transacting factor requirement for knirps and knirps-related Gene expression in the anterior but not in the posterior region of the Drosophila embryo [7].
• Our lack and gain-of-function experiments show that knirps and knirps-related which encode nuclear orphan receptors transcriptionally repress S-phase genes of the cell cycle required for DNA replication and that this down-regulation is crucial for gut morphogenesis [8].

Anatomical context of knrl

• The transacting factor requirement for the expression of kni and knrl is identical for the two anterior domains but different, although similar, for the posterior domain of expression in the blastoderm [7].

Other interactions of knrl

• We show that kni and knrl are expressed in similar narrow stripes corresponding to the position of the L2 primordium [3].

References