Ratnasinghe Brian D, Haque Neshatul, Wagenknecht Jessica B, Jensen Davin R, Esparza Guadalupe V, Leverence Elise N, De Assuncao Thiago Milech, Mathison Angela J, Lomberk Gwen, Smith Brian C, Volkman Brian F, Urrutia Raul, Zimmermann Michael T
Bioinformatics Research and Development Laboratory, Linda T. and John A. Mellowes Center for Genomic Sciences and Precision Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Department of Biochemistry, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
bioRxiv. 2023 Apr 28:2023.04.28.536249. doi: 10.1101/2023.04.28.536249.
Current capabilities in genomic sequencing outpace functional interpretations. Our previous work showed that 3D protein structure calculations enhance mechanistic understanding of genetic variation in sequenced tumors and patients with rare diseases. The KRAS GTPase is among the critical genetic factors driving cancer and germline conditions. Because KRAS-altered tumors frequently harbor one of three classic hotspot mutations, nearly all studies have focused on these mutations, leaving significant functional ambiguity across the broader KRAS genomic landscape observed in cancer and non-cancer diseases. Herein, we extend structural bioinformatics with molecular simulations to study an expanded landscape of 86 KRAS mutations. We identify multiple coordinated changes strongly associated with experimentally established KRAS biophysical and biochemical properties. The patterns we observe span hotspot and non-hotspot alterations, which can all dysregulate Switch regions, producing mutation-restricted conformations with different effector binding propensities. We experimentally measured mutation thermostability and identified shared and distinct patterns with simulations. Our results indicate mutation-specific conformations which show potential for future research into how these alterations reverberate into different molecular and cellular functions. The data we present is not predictable using current genomic tools, demonstrating the added functional information derived from molecular simulations for interpreting human genetic variation.
目前基因组测序的能力超过了功能解读。我们之前的研究表明,三维蛋白质结构计算可增强对测序肿瘤和罕见病患者基因变异的机制理解。KRAS GTP酶是驱动癌症和种系疾病的关键遗传因素之一。由于KRAS改变的肿瘤经常携带三种经典热点突变之一,几乎所有研究都集中在这些突变上,在癌症和非癌症疾病中观察到的更广泛的KRAS基因组格局中留下了显著的功能模糊性。在此,我们通过分子模拟扩展结构生物信息学,以研究86种KRAS突变的扩展格局。我们识别出与实验确定的KRAS生物物理和生化特性密切相关的多个协同变化。我们观察到的模式涵盖热点和非热点改变,这些改变都可能失调开关区域,产生具有不同效应器结合倾向的突变限制构象。我们通过实验测量了突变热稳定性,并通过模拟确定了共享和不同的模式。我们的结果表明了突变特异性构象,这为未来研究这些改变如何影响不同的分子和细胞功能显示出潜力。我们提供的数据无法用当前的基因组工具预测,这证明了分子模拟为解释人类基因变异提供的额外功能信息。