Phenotypic and Epigenetic Inheritance Across Multiple Generations in Mammals Through the Female Line

Author(s):  
Samuel P. Hoile ◽  
Karen A. Lillycrop ◽  
Leonie R. Grenfell ◽  
Mark A. Hanson ◽  
Graham C. Burdge
2019 ◽  
Vol 12 ◽  
pp. 251686571984421 ◽  
Author(s):  
Rachel M Woodhouse ◽  
Alyson Ashe

It is now clear that heredity is not determined purely by Mendelian genetic inheritance; sometimes, epigenetic signals can be passed from parent to progeny for multiple generations. This phenomenon is termed transgenerational epigenetic inheritance (TEI), and examples have now been observed in multiple organisms including plants, flies, mice, and nematodes. Here we discuss the recent findings that TEI is a multi-step process and that the putative chromatin modifiers SET-25 and SET-32 are important in the establishment but not maintenance of silencing.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Evan H. Lister-Shimauchi ◽  
Michael Dinh ◽  
Paul Maddox ◽  
Shawn Ahmed

AbstractDeficiency for telomerase results in transgenerational shortening of telomeres. However, telomeres have no known role in transgenerational epigenetic inheritance. C. elegans Protection Of Telomeres 1 (Pot1) proteins form foci at the telomeres of germ cells that disappear at fertilization and gradually accumulate during development. We find that gametes from mutants deficient for Pot1 proteins alter levels of telomeric foci for multiple generations. Gametes from pot-2 mutants give rise to progeny with abundant POT-1::mCherry and mNeonGreen::POT-2 foci throughout development, which persists for six generations. In contrast, gametes from pot-1 mutants or pot-1; pot-2 double mutants induce diminished Pot1 foci for several generations. Deficiency for MET-2, SET-25, or SET-32 methyltransferases, which promote heterochromatin formation, results in gametes that induce diminished Pot1 foci for several generations. We propose that C. elegans POT-1 may interact with H3K9 methyltransferases during pot-2 mutant gametogenesis to induce a persistent form of transgenerational epigenetic inheritance that causes constitutively high levels of heterochromatic Pot1 foci.


Author(s):  
Thushara Thamban ◽  
Viplove Agarwaal ◽  
Amitava Basu ◽  
Ramisetti Rajeev ◽  
Anunay Sinha ◽  
...  

2014 ◽  
Vol 56 ◽  
pp. 207-219 ◽  
Author(s):  
Chi L.L. Pham ◽  
Ann H. Kwan ◽  
Margaret Sunde

Amyloids are insoluble fibrillar protein deposits with an underlying cross-β structure initially discovered in the context of human diseases. However, it is now clear that the same fibrillar structure is used by many organisms, from bacteria to humans, in order to achieve a diverse range of biological functions. These functions include structure and protection (e.g. curli and chorion proteins, and insect and spider silk proteins), aiding interface transitions and cell–cell recognition (e.g. chaplins, rodlins and hydrophobins), protein control and storage (e.g. Microcin E492, modulins and PMEL), and epigenetic inheritance and memory [e.g. Sup35, Ure2p, HET-s and CPEB (cytoplasmic polyadenylation element-binding protein)]. As more examples of functional amyloid come to light, the list of roles associated with functional amyloids has continued to expand. More recently, amyloids have also been implicated in signal transduction [e.g. RIP1/RIP3 (receptor-interacting protein)] and perhaps in host defence [e.g. aDrs (anionic dermaseptin) peptide]. The present chapter discusses in detail functional amyloids that are used in Nature by micro-organisms, non-mammalian animals and mammals, including the biological roles that they play, their molecular composition and how they assemble, as well as the coping strategies that organisms have evolved to avoid the potential toxicity of functional amyloid.


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.


Author(s):  
Sara Awartani

In late September 2018, multiple generations of Chicago’s storied social movements marched through Chicago’s Lincoln Park neighborhood as part of the sold-out, three-day Young Lords Fiftieth Anniversary Symposium hosted by DePaul University—an institution that, alongside Mayor Richard J. Daley’s administration, had played a sizeable role in transforming Lincoln Park into a neighborhood “primed for development.” Students, activists, and community members—from throughout Chicago, the Midwest, the East Coast, and even as far as Texas—converged to celebrate the history of Puerto Ricans in Chicago, the legacies of the Young Lords, and the promises and possibilities of resistance. As Elaine Brown, former chairwoman and minister of information for the Black Panther Party, told participants in the second day’s opening plenary, the struggle against racism, poverty, and gentrification and for self-determination and the general empowerment of marginalized people is a protracted one. “You have living legends among you,” Brown insisted, inviting us to associate as equals with the Young Lords members in our midst. Her plea encapsulated the ethos of that weekend’s celebrations: “If we want to be free, let us live the light of the Lords.”


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