Formula G1: Cell cycle in the driver's seat of stem cell fate determination

Julian, Lisa M.; Carpenedo, Richard L.; Rothberg, Janet L. Manias; Stanford, William L.

doi:10.1002/bies.201500187

Cited by 19 publications

(12 citation statements)

References 68 publications

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“…CDK4 and its homolog CDK6 are activated by D-type cyclins in early to mid-G1 phase, whereas CDK2 is activated by E- and A-type cyclins during the late G1 and S phases, respectively [7]. Recent evidence indicates that cell-cycle dynamics have emerged as a key regulator of stem cell fate decisions [8–10]. Specifically, Cyclin D proteins have been shown to activate CDK4/6, which restricts the activity of Sma- and Mad-related Protein (Smad) 2/3 in late G1 phase and results in a switch from endoderm to neuroectoderm potential in human pluripotent stem cells [11].…”

Section: Introductionmentioning

confidence: 99%

Chemokine signaling links cell-cycle progression and cilia formation for left–right symmetry breaking

Zhu

Guan

et al. 2019

PLoS Biol

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Zebrafish dorsal forerunner cells (DFCs) undergo vigorous proliferation during epiboly and then exit the cell cycle to generate Kupffer’s vesicle (KV), a ciliated organ necessary for establishing left–right (L–R) asymmetry. DFC proliferation defects are often accompanied by impaired cilia elongation in KV, but the functional and molecular interaction between cell-cycle progression and cilia formation remains unknown. Here, we show that chemokine receptor Cxcr4a is required for L–R laterality by controlling DFC proliferation and KV ciliogenesis. Functional analysis revealed that Cxcr4a accelerates G1/S transition in DFCs and stabilizes forkhead box j1a (Foxj1a), a master regulator of motile cilia, by stimulating Cyclin D1 expression through extracellular regulated MAP kinase (ERK) 1/2 signaling. Mechanistically, Cyclin D1–cyclin-dependent kinase (CDK) 4/6 drives G1/S transition during DFC proliferation and phosphorylates Foxj1a, thereby disrupting its association with proteasome 26S subunit, non-ATPase 4b (Psmd4b), a 19S regulatory subunit. This prevents the ubiquitin (Ub)-independent proteasomal degradation of Foxj1a. Our study uncovers a role for Cxcr4 signaling in L–R patterning and provides fundamental insights into the molecular linkage between cell-cycle progression and ciliogenesis.

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Section: Introductionmentioning

confidence: 99%

Chemokine signaling links cell-cycle progression and cilia formation for left–right symmetry breaking

Zhu

Guan

et al. 2019

PLoS Biol

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“…in daughter cells shortly after NSC mitosis. This is reminiscent of embryonic stem cell differentiation that is also thought to occur in G1 (37,38), especially early G1 at a stage most favorable to massive chromatin remodeling (39). Moreover, we find 25 that this critical period is doubled in human cortical progenitors, which could contribute to their increased self-renewal capacities, thus uncovering a surprising link between mitochondria dynamics and human brain evolution.…”

Section: Main Textmentioning

confidence: 59%

Mitochondria dynamics in postmitotic cells drives neurogenesis through Sirtuin-dependent chromatin remodeling

Iwata

Vanderhaeghen

2020

Preprint

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The conversion of neural stem cells into neurons is associated with massive remodeling of organelles and chromatin, but whether and how these are linked to control neuronal fate commitment remains unknown. We examined and manipulated mitochondria dynamics with high temporal resolution during mouse and human cortical neurogenesis. We reveal that shortly after cortical stem cells have divided, daughter cells that retain high levels of mitochondria fission will become neurons, while those destined to self-renew undergo rapid mitochondria fusion. Induction of mitochondria fusion after mitosis redirects daughter cells towards cell self-renewal, but only during a restricted time window, which is doubled in human cortical stem cells with higher self-renewing potential. Mitochondria dynamics drives neurogenesis through modulation of the NAD+ sensor Sirtuin-1, leading to Histone deacetylation and chromatin remodeling necessary for neurogenic conversion. Our data reveal a post-mitotic critical period of neurogenesis, linking mitochondria state with cell fate.

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“…Using this approximation, these analyses showed that as developmental time progresses, the proliferation rate of neural progenitors decreases and their cell cycle lengthens (Molina and Pituello, 2017;Kicheva and Briscoe, 2015;Kicheva, et al, 2014). This evolution of the cell cycle length most often associated with differentiation was also observed in various stem cell types (Julian, et al, 2016;Dalton, 2015). suggesting that indeed cell cycle phase durations are stochastic and independent.…”

Section: The Lengthening Of the Cell Cycle Results From Enhanced Hetementioning

confidence: 89%

G1 Phase Lengthening During Neural Tissue Development Involves CDC25B Induced G1 Heterogeneity

Delgado¹,

Frédéric²,

Lobjois³

et al. 2020

Preprint

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While lengthening of the cell cycle and G1 phase is a generic feature of tissue maturation during development, the underlying mechanism remains still poorly understood. Here we develop a time lapse imaging strategy to measure the four phases of the cell cycle in single neural progenitor cells in their endogenous environment. Our results show that neural progenitors possess a great heterogeneity of the cell cycle length. This duration variability is distributed over all phases of the cell cycle, with the G1 phase being the one contributing primarily to cell cycle variability. Within one cell cycle, each phase duration appears stochastic and independent except for a surprising correlation between S and M phase. Lineage analysis indicates that the majority of daughter cells display longer G1 phase than their mother s suggesting that at each cell cycle a mechanism lengthens the G1 phase. We identify an actor of the core cell cycle machinery, the CDC25B phosphatase known to regulate G2/M transition, as an indirect regulator of the duration of the G1 phase. We propose that CDC25B acts via a cell to cell increase in G1 phase heterogeneity revealing a novel mechanism of G1 lengthening associated with tissue development.

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Formula G1: Cell cycle in the driver's seat of stem cell fate determination

Cited by 19 publications

References 68 publications

Chemokine signaling links cell-cycle progression and cilia formation for left–right symmetry breaking

Chemokine signaling links cell-cycle progression and cilia formation for left–right symmetry breaking

Mitochondria dynamics in postmitotic cells drives neurogenesis through Sirtuin-dependent chromatin remodeling

G1 Phase Lengthening During Neural Tissue Development Involves CDC25B Induced G1 Heterogeneity

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