Molecular mechanisms of transgenerational epigenetic inheritance

Author(s):  
Maximilian H. Fitz-James ◽  
Giacomo Cavalli
2020 ◽  
Vol 48 (3) ◽  
pp. 1019-1034 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Alyson Ashe

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.


2017 ◽  
Vol 63 (4) ◽  
pp. 173-179 ◽  
Author(s):  
Dušan Gömöry ◽  
Matúš Hrivnák ◽  
Diana Krajmerová ◽  
Roman Longauer

AbstractThe study reviews trait inheritance, which is in contradiction with the rules of Mendelian genetics, and which was object of controversies among biologists (sometimes with grave political consequences) in the USSR and Sovietcontrolled countries in the 1930s-1960s. “Carryover” or “memory” effects of the climate, to which maternal trees are exposed during seed development, on phenological behavior and other adaptively relevant traits of their offspring in conifers are mentioned; similar effects are associated with the germination and early growth environment. Molecular mechanisms underlying these effects include covalent modifications of DNA or DNA-associated proteins (cytosine methylation, various types of histone modifications), micro-RNAs and small interfering RNAs. Tools for the identification of these modifications are reviewed with a focus on cytosine methylation, along with an overview of the hitherto knowledge on the occurrence of DNA modifications in forest trees. The practical implications of epigenetic inheritance in forest trees are discussed with the focus on the adaptation to climate change and legislation on forest reproductive materials.


Cell Reports ◽  
2018 ◽  
Vol 25 (8) ◽  
pp. 2259-2272.e5 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Gabriele Buchmann ◽  
Matthew Hoe ◽  
Dylan J. Harney ◽  
Jason K.K. Low ◽  
...  

2014 ◽  
Vol 25 (23) ◽  
pp. 3726-3739 ◽  
Author(s):  
Chao Yu Zhen ◽  
Huy Nguyen Duc ◽  
Marko Kokotovic ◽  
Christopher J. Phiel ◽  
Xiaojun Ren

Polycomb group (PcG) proteins are epigenetic transcriptional factors that repress key developmental regulators and maintain cellular identity through mitosis via a poorly understood mechanism. Using quantitative live-cell imaging in mouse ES cells and tumor cells, we demonstrate that, although Polycomb repressive complex (PRC) 1 proteins (Cbx-family proteins, Ring1b, Mel18, and Phc1) exhibit variable capacities of association with mitotic chromosomes, Cbx2 overwhelmingly binds to mitotic chromosomes. The recruitment of Cbx2 to mitotic chromosomes is independent of PRC1 or PRC2, and Cbx2 is needed to recruit PRC1 complex to mitotic chromosomes. Quantitative fluorescence recovery after photobleaching analysis indicates that PRC1 proteins rapidly exchange at interphasic chromatin. On entry into mitosis, Cbx2, Ring1b, Mel18, and Phc1 proteins become immobilized at mitotic chromosomes, whereas other Cbx-family proteins dynamically bind to mitotic chromosomes. Depletion of PRC1 or PRC2 protein has no effect on the immobilization of Cbx2 on mitotic chromosomes. We find that the N-terminus of Cbx2 is needed for its recruitment to mitotic chromosomes, whereas the C-terminus is required for its immobilization. Thus these results provide fundamental insights into the molecular mechanisms of epigenetic inheritance.


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