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Beyond Mendelian Inheritance:Genetic Buffering and Phenotype Variability

Phenomics 2022年第2期2卷 79-87页

作者： Andrea Rossi Zacharias Kontarakis Genome Engineering and Model Development Lab(GEMD) IUF-Leibniz Research Institute for Environmental Medicine40225 DüsseldorfGermany Genome Engineering and Measurement Laboratory(GEML) Eidgenössische Technische Hochschule(ETH)ZurichZurichSwitzerland Functional Genomics Center Zurich of ETH Zurich University of Zurich8093 ZurichSwitzerland

Understanding the way genes work amongst individuals and across generations to shape form and function is a common theme for many genetic *** recent advances in genetics,genome engineering and DNA sequencing reinforced the notion that genes are not the only players that determine a *** to physiological or pathological fluctuations in gene expression,even genetically identical cells can behave and manifest different phenotypes under the same ***,we discuss mechanisms that can influence or even disrupt the axis between genotype and phenotype;the role of modifier genes,the general concept of genetic redundancy,genetic compensation,the recently described transcriptional adaptation,environmental stressors,and phenotypic *** furthermore highlight the usage of induced pluripotent stem cells(iPSCs),the generation of isogenic lines through genome engineering,and sequencing technologies can help extract new genetic and epigenetic mechanisms from what is hitherto considered‘noise’.

关键词： Genetic compensation transcriptional adaptation Modifiers Phenotypes Phenotypic plasticity

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Incorporation of a histone mutant with H3K56 site substitution perturbs the replication machinery in mouse embryonic stem cells

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Journal of Molecular Cell Biology 2022年第3期14卷 23-35页

作者： Xuan Kang Xiaomei Yang Xiaobo Guo Yabin Li Chenxin Yang Huimin Wei Jianfeng Chang Research Center for Translational Medicine East HospitalSchool of Life Sciences and TechnologyTongji UniversityShanghai 200092China Tsingdao Advanced Research Institute Tongji UniversityQingdao 266071China

Sense mutations in several conserved modifiable sites of histone H3 have been found to be strongly correlated with multiple tissuespecific clinical *** clinical site mutants acquire a distinctively new epigenetic role and mediate cancer *** this study,we mimicked histone H3 at the 56th lysine(H3K56)mutant incorporation in mouse embryonic stem cells(mESCs)by lentivirus-mediated ectopic expression and analyzed the effects on replication and epigenetic *** data show that two types of H3K56 mutants,namely H3 lysine 56-to-methionine(H3K56M)and H3 lysine 56-to-alanine(H3K56A),promote replication by recruiting more minichromosome maintenance complex component 3 and checkpoint kinase 1 onto chromatin compared with wild-type histone H3 and other site substitution *** this condition,the frequency of genomic copy number gain in H3K56M and H3K56A cells globally increases,especially in the Mycl1 region,a known molecular marker frequently occurring in multiple malignant ***,we found the disruption of H3K56 acetylation distribution in the copy-gain regions,which indicates a probable epigenetic mechanism of H3K56M and *** then identified that H3K56M and H3K56A can trigger a potential adaptation to transcription;genes involved in the mitogen-activated protein kinase pathway are partially upregulated,whereas genes associated with intrinsic apoptotic function show obvious *** final outcome of ectopic H3K56M and H3K56A incorporation in mESCs is an enhanced ability to form *** work indicates that H3K56 site conservation and proper modification play important roles in harmonizing the function of the replication machinery in mESCs.

关键词： H3K56A/M mutants replication promotion replication stress transcriptional adaptation mouse embryonic stem cells

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