Summary The homeodomain (HD) protein Bicoid (Bcd) is thought to function as a gradient morphogen that positions boundaries of target genes via threshold-dependent activation mechanisms. Here we analyze 66 Bcd-dependent regulatory elements, and show that their boundaries are positioned primarily by repressive gradients that antagonize Bcd-mediated activation. A major repressor is the pair-rule protein Runt, which is expressed in an opposing gradient, and is necessary and sufficient for limiting Bcd-dependent activation. Evidence is presented that Runt functions with the maternal repressor Capicua and the gap protein Kruppel as the principal components of a repression system that correctly orders boundaries throughout the anterior half of the embryo. These results put conceptual limits on the Bcd morphogen hypothesis, and demonstrate how the Bcd gradient functions within the gene network that patterns the embryo.

Purpose. To present a case of acute idiopathic maculopathy (AIM) and illustrate primary choroidal perfusion defect using multimodal imaging. Case Description. We report a case of a 24-year-old man with a paracentral scotoma of the right eye and recent flu-like illness. The patient was found to have a unilateral ovoid-shaped, placoid lesion just inferior to the fovea. Multimodal imaging confirmed findings most consistent with a diagnosis of acute idiopathic maculopathy (AIM). Serologic studies confirmed a strongly positive immunoglobulin G (IgG) titer for coxsackievirus A. Spectral-domain optical coherence tomography angiography (SD-OCTA) showed bilateral areas of vascular reduction at the level of the choriocapillaris and choroid, sparing the retinal circulation. Conclusions and Importance. The changes in outer retina and retinal pigment epithelium, classically described in AIM, are likely secondary to choroidal hypoperfusion.