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@ARTICLE{Geerds:646220,
author = {Geerds, Christina and Niemann, Hartmut},
title = {{S}ingle mutations to tyrosine or glutamate improve the
crystallizability and crystal diffraction properties of a
flexible two-domain protein},
journal = {Acta crystallographica / Section F},
volume = {82},
number = {1},
issn = {1744-3091},
address = {Oxford [u.a.]},
publisher = {Blackwell},
reportid = {PUBDB-2026-00765},
pages = {4 - 13},
year = {2026},
abstract = {This case report describes single surface substitutions
that improve the crystallizability and diffraction
properties of a flexible two-domain protein. InlB392
comprises the internalin domain and the B repeat of the
Listeria monocytogenes invasion protein InlB. The InlB392
wild type yielded very few poorly reproducible hits in
crystallization screens and the crystals had a diffraction
limit of worse than 3.0 Å. It seems reasonable to assume
that this crystallization bottleneck is caused by
interdomain flexibility, given that crystals of the isolated
internalin domain or B repeat diffract to high resolution. A
previously identified variant, T332E, showed improved
crystallization and diffraction. Here, two additional
InlB392 variants are described with single
threonine-to-tyrosine or valine-to-glutamate substitutions
that produced crystals directly in initial screens and,
without optimization, diffracted to 1.6 and 1.45 Å
resolution, respectively. The mutated residues do not
participate in intramolecular interdomain interactions but
mediate crystal contacts, indicating that specific surface
properties, rather than interdomain flexibility per se,
impede the crystallization of wild-type InlB392. Notably,
the beneficial glutamate substitutions contrast with the
generally recognized underrepresentation of glutamate in
crystal contacts and the high entropic cost of fixing an
otherwise flexible side chain with many rotatable bonds in a
crystal contact. The reported results suggest that surface
mutations can help crystallization even if they increase the
entropy of the respective residue. More broadly, the
observations are consistent with the hypothesis that
negative evolutionary design limits fortuitous lattice
formation of proteins and the resulting expectation that
random mutations of surface residues are likely to improve
crystallizability.},
cin = {EMBL-User},
ddc = {530},
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-P13-20150101},
typ = {PUB:(DE-HGF)16},
doi = {10.1107/S2053230X25010416},
url = {https://bib-pubdb1.desy.de/record/646220},
}