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. 2021 Sep 21;9:715868. doi: 10.3389/fcell.2021.715868

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Copyright © 2021 Giordano, Pirone, Muratore, Landaluze, Pérez, Lang, Garde-Lapido, Gonzalez-Lopez, Barroso-Gomila, Vertegaal, Aransay, Rodriguez, Rodriguez, Sutherland and Barrio.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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SALL1 influences regulation of CBX4 target genes. Hypothetical model showing speculative scenarios whereby SALL1 could influence CBX4-mediated regulation of target genes. Binding to SALL1 (SUMOylated or non-SUMOylated) could stabilize CBX4 by interfering with its ubiquitination and its consequent degradation by the proteasome. CBX4 stabilization entails an increment of its protein levels and its accumulation in Pc bodies. Binding to SUMOylated SALL1 increases CBX4-mediated transcriptional repression of its target genes. At least two non-exclusive hypothetical mechanisms might underlie this effect. Under one hypothetical scenario (left side), it could be due to the concurrent recruitment of other essential cofactors. In another hypothetical scenario (right side), SUMOylated SALL1 could increase CBX4 transcriptional repression by facilitating its SUMOylation through recruitment of SUMOylation machinery components. Discontinuous arrows indicate speculative events that have not been proven experimentally.