Growth of the Developing Cerebral Cortex Is Controlled by MicroRNA-7 through the p53 Pathway

Pollock, Andrew; Bian, Shan; Zhang, Chao; Chen, Zhengming; Sun, Tao

doi:10.1016/j.celrep.2014.04.003

Cited by 81 publications

(60 citation statements)

References 46 publications

(52 reference statements)

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“…Previous studies in rodent models found that P53-induced apoptosis is responsible for neuronal loss in many different congenital microcephalies. 32, 51, 52, 53, 54, 55 In some of these cases, P53 activation was correlated with increased DNA damage accumulation. 32, 52, 54, 55 The recent report that DNA damage and consequent P53 activation can result from increased mitosis length in neural progenitors 32 suggests that this mechanism could be much more common in microcephaly than previously thought, because many microcephaly genes have the potential to impact on mitosis timing.…”

Section: Discussionmentioning

confidence: 97%

ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly and p53

et al. 2016

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Epidemiological evidence from the current outbreak of Zika virus (ZIKV) and recent studies in animal models indicate a strong causal link between ZIKV and microcephaly. ZIKV infection induces cell-cycle arrest and apoptosis in proliferating neural progenitors. However, the mechanisms leading to these phenotypes are still largely obscure. In this report, we explored the possible similarities between transcriptional responses induced by ZIKV in human neural progenitors and those elicited by three different genetic mutations leading to severe forms of microcephaly in mice. We found that the strongest similarity between all these conditions is the activation of common P53 downstream genes. In agreement with these observations, we report that ZIKV infection increases total P53 levels and nuclear accumulation, as well as P53 Ser15 phosphorylation, correlated with genotoxic stress and apoptosis induction. Interestingly, increased P53 activation and apoptosis are induced not only in cells expressing high levels of viral antigens but also in cells showing low or undetectable levels of the same proteins. These results indicate that P53 activation is an early and specific event in ZIKV-infected cells, which could result from cell-autonomous and/or non-cell-autonomous mechanisms. Moreover, we highlight a small group of P53 effector proteins that could act as critical mediators, not only in ZIKV-induced microcephaly but also in many genetic microcephaly syndromes.

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Section: Discussionmentioning

confidence: 97%

ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly and p53

et al. 2016

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“…MicroRNAs (miRNAs) have emerged as important regulators of NPC proliferation and neocortex size [66][67][68][69][70][71][72].…”

Section: Micrornasmentioning

confidence: 99%

Human-specific genomic signatures of neocortical expansion

Florio

Borrell

Huttner

2017

Current Opinion in Neurobiology

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“…For example, circRNA Cdr1as is expressed exclusively in the brain and has more than 70 binding sites for miR-7, 59,60 which in turn regulates many other genes in the brain. 61–63 CDR1as may act like a sponge for miR-7, 59,60 and animals with a genetic disruption of Cdr1as had deficits in neurotransmission. 64 …”

Section: Rna Modificationsmentioning

confidence: 99%

Role of RNA modifications in brain and behavior

Jung

Goldman

2018

Genes Brain and Behavior

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Much progress in our understanding of RNA metabolism has been made since the first RNA nucleoside modification was identified in 1957. Many of these modifications are found in noncoding RNAs but recent interest has focused on coding RNAs. Here, we summarize current knowledge of cellular consequences of RNA modifications, with a special emphasis on neuropsychiatric disorders. We present evidence for the existence of an “RNA code,” similar to the histone code, that fine-tunes gene expression in the nervous system by using combinations of different RNA modifications. Unlike the relatively stable genetic code, this combinatorial RNA epigenetic code, or epitranscriptome, may be dynamically reprogrammed as a cause or consequence of psychiatric disorders. We discuss potential mechanisms linking disregulation of the epitranscriptome with brain disorders and identify potential new avenues of research.

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Growth of the Developing Cerebral Cortex Is Controlled by MicroRNA-7 through the p53 Pathway

Cited by 81 publications

References 46 publications

ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly and p53

ZIKA virus elicits P53 activation and genotoxic stress in human neural progenitors similar to mutations involved in severe forms of genetic microcephaly and p53

Human-specific genomic signatures of neocortical expansion

Role of RNA modifications in brain and behavior

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