Journal ArticleDOI
Myc-driven endogenous cell competition in the early mammalian embryo
TLDR
It is shown that natural cell competition in the early mammalian embryo contributes to the selection of the epiblast cell pool through the elimination of cells with low relative Myc levels.Abstract:
The epiblast is the mammalian embryonic tissue that contains the pluripotent stem cells that generate the whole embryo. We have established a method for inducing functional genetic mosaics in the mouse. Using this system, here we show that induction of a mosaic imbalance of Myc expression in the epiblast provokes the expansion of cells with higher Myc levels through the apoptotic elimination of cells with lower levels, without disrupting development. In contrast, homogeneous shifts in Myc levels did not affect epiblast cell viability, indicating that the observed competition results from comparison of relative Myc levels between epiblast cells. During normal development we found that Myc levels are intrinsically heterogeneous among epiblast cells, and that endogenous cell competition refines the epiblast cell population through the elimination of cells with low relative Myc levels. These results show that natural cell competition in the early mammalian embryo contributes to the selection of the epiblast cell pool.read more
Citations
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Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy
TL;DR: The biochemical, structural and genetic studies that have clarified how the interplay between members of the BCL-2 family on mitochondria sets the apoptotic threshold are discussed, illuminating the physiological control of apoptosis, the pathological consequences of its dysregulation and the promising search for novel cancer therapies that target the BCA2 protein family.
Journal ArticleDOI
BCL-2 proteins and apoptosis: Recent insights and unknowns.
TL;DR: Insight into BAX/BAK shuttling, BCL-2 protein interactions, the role of BH3-only proteins in apoptosis signaling and the active BAX complex set the stage for the development of novel strategies in cancer therapy and the analysis of cellular predisposition to apoptosis.
Journal ArticleDOI
New insights into the generation and role of de novo mutations in health and disease.
TL;DR: De novo mutations have been shown to be a major cause of severe early-onset genetic disorders such as intellectual disability, autism spectrum disorder, and other developmental diseases.
Journal ArticleDOI
Promoter of lncRNA Gene PVT1 Is a Tumor-Suppressor DNA Boundary Element
Seung Woo Cho,Jin Xu,Ruping Sun,Maxwell R. Mumbach,Ava C. Carter,Y. Grace Chen,Kathryn E. Yost,Jeewon Kim,Jing He,Stephanie A. Nevins,Suet-Feung Chin,Carlos Caldas,Carlos Caldas,S. John Liu,Max A. Horlbeck,Daniel A. Lim,Daniel A. Lim,Jonathan S. Weissman,Christina Curtis,Howard Y. Chang +19 more
TL;DR: It is shown that the PVT1 promoter has a tumor-suppressor function that is independent of PVT 1 lnc RNA, and regulatory sequences of lncRNA genes as potential disease-associated DNA elements are highlighted.
Journal ArticleDOI
Physical traits of cancer.
TL;DR: The authors provide a conceptual framework and discuss the origins of these distinct physical traits of cancer and how they enable and synergize with aberrant cancer biology to fuel cancer initiation, progression, immune evasion, and treatment resistance.
References
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Book
Mixed-Effects Models in S and S-PLUS
TL;DR: Linear Mixed-Effects and Nonlinear Mixed-effects (NLME) models have been studied in the literature as mentioned in this paper, where the structure of grouped data has been used for fitting LME models.
Journal ArticleDOI
Cre reporter strains produced by targeted insertion of EYFP and ECFP into the ROSA26 locus
Shankar Srinivas,Tomoko Watanabe,Chyuan-Sheng Lin,Chris M William,Yasuto Tanabe,Thomas M. Jessell,Frank Costantini +6 more
TL;DR: In contrast to existing lacZ reporter lines, where lacZ expression cannot easily be detected in living tissue, the EYFP and ECFP reporter strains are useful for monitoring the expression of Cre and tracing the lineage of these cells and their descendants in cultured embryos or organs.
Journal ArticleDOI
Programmed Cell Death in Animal Development
TL;DR: Because of the limited number of references allowed, the authors were unable to cite many important papers; they apologize to their authors.
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