% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Mattiotti:638192,
author = {Mattiotti, Giovanni and Nanna, Vittoria and Giulini, Marco
and Alberga, Domenico and Mangiatordi, Giuseppe Felice and
Sánchez-Puig, Nuria and Saviano, Michele and Tubiana, Luca
and Potestio, Raffaello and Lattanzi, Gianluca and Siliqi,
Dritan},
title = {{S}tructural {I}mplications of {M}issense {P}oint
{M}utations in {S}hwachman–{B}odian–{D}iamond {S}yndrome
{P}rotein ({SBDS}): {A} {C}ombined {SAXS}/{MD}
{I}nvestigation},
journal = {ACS omega},
volume = {10},
number = {31},
issn = {2470-1343},
address = {Washington, DC},
publisher = {ACS Publications},
reportid = {PUBDB-2025-04010},
pages = {35103 - 35118},
year = {2025},
abstract = {Shwachman–Diamond syndrome (SDS) is a rare autosomal
recessive disorder characterized by pleiotropic phenotypes,
including pancreatic insufficiency, skeletal abnormalities,
and bone marrow dysfunction. Notably, patients with SDS
exhibit an increased risk of developing myelodysplastic
syndrome and leukemia. In this study, we employed a
combination of comparative molecular dynamics (MD)
simulations and small-angle X-ray scattering (SAXS)-based
analysis to investigate the Shwachman–Bodian–Diamond
syndrome protein (SBDS). Specifically, we explored the
molecular basis of the syndrome by examining the
conformational dynamics of a set of missense mutants of SBDS
in comparison to those of the wild-type (WT) protein. Our
observations suggest that different mutations may impact (i)
the interaction of SBDS with the ribosome, (ii) the binding
of SBDS to Elongation Factor-Like 1 (EFL1), and (iii) the
SBDS rearrangements coupled to EFL1 binding. Extensive MD
simulations, with a total simulation time of 17 μs,
revealed variations in the interdomain flexibility of SBDS,
which are consistent with previously published affinity data
and the new SAXS experimental data presented here. We
propose a structural rationale behind the previously
reported weak interaction of mutants I167T, R175W, and I212T
with EFL1. Additionally, SAXS data indicate that R19Q,
I167T, and R175W mutants exhibit altered relative abundances
of SBDS conformational states in solution, further
supporting our computational results. Overall, our
integrated computational and experimental approach provides
a comprehensive understanding of how specific mutations in
SBDS alter its structural dynamics and binding interactions.
These insights enhance our broader understanding of SBDS
function and its role in ribosome biogenesis.},
cin = {EMBL-User},
ddc = {660},
cid = {I:(DE-H253)EMBL-User-20120814},
pnm = {6G3 - PETRA III (DESY) (POF4-6G3)},
pid = {G:(DE-HGF)POF4-6G3},
experiment = {EXP:(DE-H253)P-P12-20150101},
typ = {PUB:(DE-HGF)16},
doi = {10.1021/acsomega.5c04764},
url = {https://bib-pubdb1.desy.de/record/638192},
}