TY - JOUR
T1 - Structural study of UFL1-UFC1 interaction uncovers the role of UFL1 N-terminal helix in ufmylation
AU - Banerjee, Sayanika
AU - Varga, Julia K.
AU - Kumar, Manoj
AU - Zoltsman, Guy
AU - Rotem-Bamberger, Shahar
AU - Cohen-Kfir, Einav
AU - Isupov, Michail N.
AU - Rosenzweig, Rina
AU - Schueler-Furman, Ora
AU - Wiener, Reuven
N1 - Publisher Copyright:
© 2023 The Authors. Published under the terms of the CC BY NC ND 4.0 license.
PY - 2023/12/6
Y1 - 2023/12/6
N2 - Ufmylation plays a crucial role in various cellular processes including DNA damage response, protein translation, and ER homeostasis. To date, little is known about how the enzymes responsible for ufmylation coordinate their action. Here, we study the details of UFL1 (E3) activity, its binding to UFC1 (E2), and its relation to UBA5 (E1), using a combination of structural modeling, X-ray crystallography, NMR, and biochemical assays. Guided by Alphafold2 models, we generate an active UFL1 fusion construct that includes its partner DDRGK1 and solve the crystal structure of this critical interaction. This fusion construct also unveiled the importance of the UFL1 N-terminal helix for binding to UFC1. The binding site suggested by our UFL1-UFC1 model reveals a conserved interface, and competition between UFL1 and UBA5 for binding to UFC1. This competition changes in the favor of UFL1 following UFM1 charging of UFC1. Altogether, our study reveals a novel, terminal helix-mediated regulatory mechanism, which coordinates the cascade of E1-E2-E3-mediated transfer of UFM1 to its substrate and provides new leads to target this modification.
AB - Ufmylation plays a crucial role in various cellular processes including DNA damage response, protein translation, and ER homeostasis. To date, little is known about how the enzymes responsible for ufmylation coordinate their action. Here, we study the details of UFL1 (E3) activity, its binding to UFC1 (E2), and its relation to UBA5 (E1), using a combination of structural modeling, X-ray crystallography, NMR, and biochemical assays. Guided by Alphafold2 models, we generate an active UFL1 fusion construct that includes its partner DDRGK1 and solve the crystal structure of this critical interaction. This fusion construct also unveiled the importance of the UFL1 N-terminal helix for binding to UFC1. The binding site suggested by our UFL1-UFC1 model reveals a conserved interface, and competition between UFL1 and UBA5 for binding to UFC1. This competition changes in the favor of UFL1 following UFM1 charging of UFC1. Altogether, our study reveals a novel, terminal helix-mediated regulatory mechanism, which coordinates the cascade of E1-E2-E3-mediated transfer of UFM1 to its substrate and provides new leads to target this modification.
KW - AlphaFold2
KW - DDRGK1
KW - UFC1
KW - UFL1
KW - ufmylation
UR - http://www.scopus.com/inward/record.url?scp=85177479543&partnerID=8YFLogxK
U2 - 10.15252/embr.202356920
DO - 10.15252/embr.202356920
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C2 - 37988244
AN - SCOPUS:85177479543
SN - 1469-221X
VL - 24
SP - 1
EP - 14
JO - EMBO Reports
JF - EMBO Reports
IS - 12
M1 - e56920
ER -