Trrap-Dependent Histone Acetylation Specifically Regulates Cell-Cycle Gene Transcription to Control Neural Progenitor Fate Decisions

Tapias, Alicia; Zhou, Zhong-Wei; Shi, Yue; Chong, Zechen; Wang, Pei; Groth, Marco; Platzer, Matthias; Huttner, Wieland B.; Herceg, Zdenko; Yang, Yun; Wang, Zhao Qi

doi:10.1016/j.stem.2014.04.001

Cited by 48 publications

(63 citation statements)

References 64 publications

(99 reference statements)

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“…We found that almost all mitotic nuclei became EdU + in the 2 h after EdU administration in both wild-type and Ptpn11-cKO embryos at E11.5 (Fig. S1A), indicating an average G2 length of <2 h, similar to that reported previously (Arai et al, 2011;Tapias et al, 2014). Given the relatively short and constant M phase of neural progenitors (0.5-1.0 h) (Arai et al, 2011;Tapias et al, 2014), we deduce that Ptpn11 deletion does not significantly change G1 duration but mainly affects the S phase.…”

Section: Discussionsupporting

confidence: 88%

“…S1A), indicating an average G2 length of <2 h, similar to that reported previously (Arai et al, 2011;Tapias et al, 2014). Given the relatively short and constant M phase of neural progenitors (0.5-1.0 h) (Arai et al, 2011;Tapias et al, 2014), we deduce that Ptpn11 deletion does not significantly change G1 duration but mainly affects the S phase. Although we did not measure cell cycle parameters, we showed that Mek1 DD expression inhibited cell cycle exit and reduced cell cycle activity in the posterior tectum (Fig.…”

Section: Discussionsupporting

confidence: 87%

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Regulation of self-renewing neural progenitors by FGF/ERK signaling controls formation of the inferior colliculus

Dee

Heng

et al. 2016

Development

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The embryonic tectum displays an anteroposterior gradient in development and produces the superior colliculus and inferior colliculus. Studies suggest that partition of the tectum is controlled by different strengths and durations of FGF signals originated from the so-called isthmic organizer at the mid/hindbrain junction; however, the underlying mechanism is unclear. We show that deleting Ptpn11, which links FGF with the ERK pathway, prevents inferior colliculus formation by depleting a previously uncharacterized stem cell zone. The stem-zone loss is attributed to shortening of S phase and acceleration of cell cycle exit and neurogenesis. Expression of a constitutively active Mek1 (Mek1 DD ), the known ERK activator, restores the tectal stem zone and the inferior colliculus without Ptpn11. By contrast, Mek1 DD expression fails to rescue the tectal stem zone and the inferior colliculus in the absence of Fgf8 and the isthmic organizer, indicating that FGF and Mek1 DD initiate qualitatively and/or quantitatively distinctive signaling. Together, our data show that the formation of the inferior colliculus relies on the provision of new cells from the tectal stem zone. Furthermore, distinctive ERK signaling mediates Fgf8 in the control of cell survival, tissue polarity and cytogenetic gradient during the development of the tectum.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 87%

Regulation of self-renewing neural progenitors by FGF/ERK signaling controls formation of the inferior colliculus

Dee

Heng

et al. 2016

Development

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“…After sufficient NPCs expansion, neurogenesis then begins, which requires switching of the cleavage plane from horizontal to vertical (Rakic, 1995; Lancaster et al , 2013). The defect in apical progenitor expansion at the ventricular zone via vertical orientation accompanied by premature neurogenesis has been shown to occur due to cell cycle delay (Calegari et al , 2005; Tapias et al , 2014). …”

Section: Resultsmentioning

confidence: 99%

CPAP promotes timely cilium disassembly to maintain neural progenitor pool

et al. 2016

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A mutation in the centrosomal‐P4.1‐associated protein (CPAP) causes Seckel syndrome with microcephaly, which is suggested to arise from a decline in neural progenitor cells (NPCs) during development. However, mechanisms of NPCs maintenance remain unclear. Here, we report an unexpected role for the cilium in NPCs maintenance and identify CPAP as a negative regulator of ciliary length independent of its role in centrosome biogenesis. At the onset of cilium disassembly, CPAP provides a scaffold for the cilium disassembly complex (CDC), which includes Nde1, Aurora A, and OFD1, recruited to the ciliary base for timely cilium disassembly. In contrast, mutated CPAP fails to localize at the ciliary base associated with inefficient CDC recruitment, long cilia, retarded cilium disassembly, and delayed cell cycle re‐entry leading to premature differentiation of patient iPS‐derived NPCs. Aberrant CDC function also promotes premature differentiation of NPCs in Seckel iPS‐derived organoids. Thus, our results suggest a role for cilia in microcephaly and its involvement during neurogenesis and brain size control.

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“…When neurogenesis begins after sufficient NPC expansion, the dividing cells change their orientation toward the lumen, and the division plane switches from horizontal to vertical (Gabriel et al, 2016;Lancaster et al, 2013;Rakic, 1995). Cell cycle delay leading to premature differentiation has been shown to be accompanied by increased proportions of vertically oriented NPCs (Calegari et al, 2005;Gabriel et al, 2016;Tapias et al, 2014). In contrast to VZs in uninfected organoids, ZIKV-infected VZs displayed increased frequencies of vertically oriented mitotic progenitors, indicating unscheduled switching of the division plane (Figures 4F-4H).…”

Section: Zikv-infected Organoids Display An Altered Division Plane Ofmentioning

confidence: 98%

Recent Zika Virus Isolates Induce Premature Differentiation of Neural Progenitors in Human Brain Organoids

et al. 2017

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SUMMARYThe recent Zika virus (ZIKV) epidemic is associated with microcephaly in newborns. Although the connection between ZIKV and neurodevelopmental defects is widely recognized, the underlying mechanisms are poorly understood. Here we show that two recently isolated strains of ZIKV, an American strain from an infected fetal brain (FB-GWUH-2016) and a closely-related Asian strain (H/PF/2013), productively infect human iPSC-derived brain organoids. Both of these strains readily target to and replicate in proliferating ventricular zone (VZ) apical progenitors. The main phenotypic effect was premature differentiation of neural progenitors associated with centrosome perturbation, even during early stages of infection, leading to progenitor depletion, disruption of the VZ, impaired neurogenesis, and cortical thinning. The infection pattern and cellular outcome differ from those seen with the extensively passaged ZIKV strain MR766. The structural changes we see after infection with these more recently isolated viral strains closely resemble those seen in ZIKV-associated microcephaly.

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Trrap-Dependent Histone Acetylation Specifically Regulates Cell-Cycle Gene Transcription to Control Neural Progenitor Fate Decisions

Cited by 48 publications

References 64 publications

Regulation of self-renewing neural progenitors by FGF/ERK signaling controls formation of the inferior colliculus

Regulation of self-renewing neural progenitors by FGF/ERK signaling controls formation of the inferior colliculus

CPAP promotes timely cilium disassembly to maintain neural progenitor pool

Recent Zika Virus Isolates Induce Premature Differentiation of Neural Progenitors in Human Brain Organoids

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