Department of Biochemistry, Microbiology and Immunology, Wayne State University School of Medicine, 540 East Canfield Street, Detroit, MI 48201, USA.
Center for Molecular and Translational Medicine, Georgia State University, Atlanta, GA 30303, USA.
Biomolecules. 2022 Jun 3;12(6):783. doi: 10.3390/biom12060783.
SMYD5 belongs to a special class of protein lysine methyltransferases with an MYND (Myeloid-Nervy-DEAF1) domain inserted into a SET (Suppressor of variegation, Enhancer of Zeste, Trithorax) domain. Despite recent advances in its functional characterization, the lack of the crystal structure has hindered our understanding of the structure-and-function relationships of this most unique member of the SMYD protein family. Here, we demonstrate the reliability of using AlphaFold structures for understanding the structure and function of SMYD5 by comparing the AlphaFold structures to the known crystal structures of SMYD proteins, using an inter-residue distance maps-based metric. We found that the AlphaFold confidence scores are inversely associated with the refined B-factors and can serve as a structural indicator of conformational flexibility. We also found that the N-terminal sequence of SMYD5, predicted to be a mitochondrial targeting signal, contains a novel non-classical nuclear localization signal. This sequence is structurally flexible and does not have a well-defined conformation, which might facilitate its recognition for SMYD5's cytonuclear transport. The structure of SMYD5 is unique in many aspects. The "crab"-like structure with a large negatively charged cleft provides a potential binding site for basic molecules such as protamines. The less positively charged MYND domain is associated with the undetectable DNA-binding ability. The most surprising feature is an incomplete target lysine access channel that lacks the evolutionarily conserved tri-aromatic arrangement, being associated with the low H3/H4 catalytic activity. This study expands our understanding of the SMYD protein family from a classical two-lobed structure to a structure of its own kind, being as a fundamental determinant of its functional divergence.
SMYD5 属于一种特殊的蛋白赖氨酸甲基转移酶,其 MYND(髓系-神经-耳聋 1)结构域插入 SET(变异抑制、增强子结合锌指蛋白、果蝇 trithorax)结构域中。尽管最近在其功能表征方面取得了进展,但缺乏晶体结构阻碍了我们对这个 SMYD 蛋白家族中最独特成员的结构-功能关系的理解。在这里,我们通过比较 AlphaFold 结构与已知的 SMYD 蛋白晶体结构,使用基于残基间距离图的度量标准,证明了使用 AlphaFold 结构来理解 SMYD5 的结构和功能的可靠性。我们发现 AlphaFold 的置信得分与精修 B 因子呈反比,可作为构象灵活性的结构指标。我们还发现,SMYD5 的 N 端序列(预测为线粒体靶向信号)包含一个新的非经典核定位信号。该序列结构灵活,没有明确的构象,这可能有助于其识别 SMYD5 的细胞质核运输。SMYD5 的结构在许多方面都是独特的。带有大的带负电荷裂缝的“蟹”状结构提供了一个潜在的结合碱性分子如鱼精蛋白的位点。带较少正电荷的 MYND 结构域与不可检测的 DNA 结合能力相关。最令人惊讶的特征是一个不完整的靶赖氨酸进入通道,缺乏进化上保守的三芳基排列,与低 H3/H4 催化活性相关。这项研究从经典的两叶结构扩展了我们对 SMYD 蛋白家族的理解,到一种自身结构,成为其功能分化的基本决定因素。