Cell Turnover and Adult Tissue Homeostasis: From Humans to Planarians

Pellettieri, Jason; Alvarado, Alejandro Sánchez

doi:10.1146/annurev.genet.41.110306.130244

Cited by 285 publications

(241 citation statements)

References 94 publications

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“…growth), most animal species exhibit cell renewal and tissue repair. All these processes rely on the combination of cell proliferation, cell death and cell differentiation but whereas tissue repair and regeneration are induced upon external forces (injury, tissue damage, amputation), cell renewal rather responds to an endogenous regulation 4 .…”

Section: Apoptosis-induced Compensatory Proliferationmentioning

confidence: 99%

The Hydra model: disclosing an apoptosis-driven generator of Wnt-based regeneration

Galliot

Chera²

2010

Trends in Cell Biology

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The Hydra model system is well suited to decipher the mechanisms underlying adult regeneration, opening the possibility to characterize those that have been robust enough to be maintained across evolutionary time. The detailed analysis of the activation of the Wnt-βcatenin pathway in bisected Hydra actually shows that the route taken to regenerate a structure as complex as the head dramatically varies according to the amputation level. When decapitation induces a direct redevelopment thanks to Wnt3 signaling from the epithelial cells, head regeneration after midgastric section relies first on Wnt3 signaling from the interstitial cells that undergo apoptosis-induced compensatory proliferation and secondarily activate Wnt3 signaling in the epithelial cells. The relative distribution between stem cells and head progenitor cells is strikingly different in these two contexts indicating that the pre-amputation homeostatic conditions define and constrain the route that bridges wound healing to the re-development program of the missing structure.

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Section: Apoptosis-induced Compensatory Proliferationmentioning

confidence: 99%

The Hydra model: disclosing an apoptosis-driven generator of Wnt-based regeneration

Galliot

Chera²

2010

Trends in Cell Biology

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“…Once the muscle has matured, these progenitors will enter quiescence and henceforth reside within in it as satellite cells. Adult skeletal muscle, like all renewing organs, relies on a mechanism that compensates for the turnover of terminally differentiated cells to maintain tissue homeostasis (Schmalbruch and Lewis 2000;Pellettieri and Sanchez Alvarado 2007). This type of myogenesis depends on the activation of satellite cells that have the potential to differentiate into new fibers (Charge and Rudnicki 2004).…”

Section: Introductionmentioning

confidence: 99%

Building Muscle: Molecular Regulation of Myogenesis

Bentzinger¹,

Wang²,

Rudnicki³

2012

Cold Spring Harbor Perspectives in Biology

918

878

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SUMMARYThe genesis of skeletal muscle during embryonic development and postnatal life serves as a paradigm for stem and progenitor cell maintenance, lineage specification, and terminal differentiation. An elaborate interplay of extrinsic and intrinsic regulatory mechanisms controls myogenesis at all stages of development. Many aspects of adult myogenesis resemble or reiterate embryonic morphogenetic episodes, and related signaling mechanisms control the genetic networks that determine cell fate during these processes. An integrative view of all aspects of myogenesis is imperative for a comprehensive understanding of muscle formation. This article provides a holistic overview of the different stages and modes of myogenesis with an emphasis on the underlying signals, molecular switches, and genetic networks.

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“…There are several mechanisms by which such dominance can emerge, e.g. by uneven starting populations in the embryo, drift, competition, interference, unequal cell proliferation or death, or a combination of these mechanisms (39)(40)(41)(42). Controlling the temporal and spatial induction of edits and isolating defined cell types from diverse organs should help resolve the mechanisms by which different embryonic progenitors come to dominate different adult organs.…”

Section: Discussionmentioning

confidence: 99%

Whole organism lineage tracing by combinatorial and cumulative genome editing

McKenna

Findlay

Gagnon

et al. 2016

Preprint

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Multicellular systems develop from single cells through distinct lineages. However, current lineage tracing approaches scale poorly to whole, complex organisms. Here we use genome editing to progressively introduce and accumulate diverse mutations in a DNA barcode over multiple rounds of cell division. The barcode, an array of CRISPR/Cas9 target sites, marks cells and enables the elucidation of lineage relationships via the patterns of mutations shared between cells. In cell culture and zebrafish, we show that rates and patterns of editing are tunable, and that thousands of lineage-informative barcode alleles can be generated. By sampling hundreds of thousands of cells from individual zebrafish, we find that most cells in adult organs derive from relatively few embryonic progenitors. In future analyses, genome editing of synthetic target arrays for lineage tracing (GESTALT) can be used to generate large-scale maps of cell lineage in multicellular systems for normal development and disease.

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Cell Turnover and Adult Tissue Homeostasis: From Humans to Planarians

Cited by 285 publications

References 94 publications

The Hydra model: disclosing an apoptosis-driven generator of Wnt-based regeneration

The Hydra model: disclosing an apoptosis-driven generator of Wnt-based regeneration

Building Muscle: Molecular Regulation of Myogenesis

Whole organism lineage tracing by combinatorial and cumulative genome editing

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