Figure: DYNLL1 binds to MRE11 to limit DNA end resection (Human).¶
This figure depicts the regulatory pathway of DNA end resection during DNA double-strand break repair. TP53BP1 (blue) recognizes modified histones at the site of double-strand breaks and recruits DYNLL1 (pink). DYNLL1 acts as an enzyme inhibitor, binding to MRE11 (green) and inhibiting both its endonuclease (GO:0004520) and 3'-5' exonuclease (GO:0008296) activities. This inhibition limits DNA end resection during replication fork processing (GO:0110025), representing a negative regulation mechanism (GO:0110027). The diagram shows these interactions occurring at the site of a DNA double-strand break (GO:0035861) within the cell nucleus. Modified histones (orange) that serve as recognition sites for TP53BP1 are included as implicit details not explicitly mentioned in the GO-CAM model but necessary for biological context.
Feedback from AI on figure:
{"feedback":"The diagram effectively illustrates the regulatory pathway of DNA end resection at double-strand breaks, highlighting key protein interactions between TP53BP1, DYNLL1, and MRE11. The spatial organization clearly shows the progression from histone recognition to DYNLL1 recruitment and subsequent inhibition of MRE11 activities. Color coding and a comprehensive legend enhance readability, with appropriately sized fonts ensuring all text is clearly visible. The inclusion of GO terms provides valuable reference information while maintaining visual clarity. The implicit detail of modified histones is appropriately marked, adding necessary biological context without compromising fidelity to the source data. Overall, this figure successfully balances scientific accuracy with visual accessibility, making it suitable for publication in high-impact journals.","necessary_changes":null,"optional_changes":null}