Gap Analysis of Standard Automated Perimetry Concept Representation in Medical Terminologies.

Classically known as a transcription factor mastering the development of the mammalian rostral brain and promoting the cytoarchitectonic maturation and activity of neocortical neurons (reviewed in Artimagnella et al., 2024), Foxg1 has been recently found to be engaged in an array of activities other than pure transcriptional control. Specifically, Foxg1 has been shown to regulate the translation of hundreds of genes, modulating the recruitment of their mRNAs to ribosomes and the progression of the latter on the former. This is associated with physical interaction between Foxg1 and specific translation factors (EIF4E and EEF1D) and can be replicated by an artificial, variant of Foxg1, confined to cytoplasm and unable to impact transcription (Artimagnella et al., 2024). Interestingly, among genes undergoing translational control by Foxg1, many are specifically involved in neuronal physiology (Artimagnella et al., 2024). Furthermore, two largely overlapping carboxyterminal fragments of Foxg1, the former generated by post-translational processing of the wild-type protein and the latter overexpressed in mutants harboring a premature stop codon, have been reported to move to mitochondria, interact with mito-ribosomal proteins and promote translation of specific mitochondrial transcripts (Bruce et al., 2024). Intriguingly, the non-transcriptional impact of Foxg1 on gene expression is not restricted to translation, but also extends to other processes, including retro-transcription (Liuzzi et al., 2024) and post-transcriptional RNA processing (Skalhegg and Tasken, 2000; Artimagnella et al., 2024). From this point of view, Foxg1 is not a unique case. In fact, well before it, several homeodomain-TF genes, mainly involved in embryo patterning had already been shown to contribute to the post-transcriptional control of gene expression. The first one was (), which encodes for a homeodomain-TF expressed in the syncytial-blastoderm of the Drosophila embryo along an anterior-to-caudal gradient, and which acts as a maternal determinant of anterior identity. As early as 1996, it was reported that, in addition to differentially promoting the transcription of three anterior gap genes, , , and (Driever and Nüsslein-Volhard, 1989; Struhl et al., 1989; Finkelstein and Perrimon, 1990), Bicoid also trans-represses the translation of the ubiquitous -mRNA, thus limiting the high expression of its protein product to the caudal-most part of the embryo (Dubnau and Struhl, 1996). Bicoid has been found to bind to a BRE-motif lying in -mRNA-3’UTR, using an arginine-rich module (ARM) located in the 3’-most part of its homeodomain (Niessing et al., 2000). Moreover, anchored to -mRNA, Bicoid further binds to EIF4E attached to -mRNA-5’cap, thanks to a YXXXXLF motif similar to those mediating the EIF4E/EIF4E-BP interaction. In this way, Bicoid prevents EIF4E interaction with EIF4G and thus impairs the translation of -mRNA (Niessing et al., 2002).