Human neuronal maturation comes of age: cellular mechanisms and species differences

Wallace, Jenelle L.; Pollen, Alex A.

doi:10.1038/s41583-023-00760-3

Cited by 3 publications

(1 citation statement)

References 273 publications

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“…Understanding how these structural differences arise during development is an intensive area of investigation (Amin and Borrell, 2020;Moffat and Schuurmans, 2023). A key distinction between human and rodent corticogenesis is the evolution of unique neural progenitor cell (NPC) pools along with temporal differences in neuronal differentiation and maturation processes (Wallace and Pollen, 2023). Human NPCs have an overall longer neurogenic period, in part due to increased protein half-lives (Rayon et al, 2020) and longer cell cycle times, which are recapitulated in differentiation assays in vitro (Herculano-Houzel, 2012;van den Ameele et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

NEUROG2regulates a human-specific neurodevelopmental gene regulatory program

Chinchalongporn,

Vasan,

Saleh

et al. 2024

Preprint

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Unique hallmarks of human neocortical development include slower rates of neurogenesis and the establishment of an extracellular matrix-rich, outer-subventricular zone that supports basal neural progenitor cell expansion. How gene regulatory networks have evolved to support these human-specific neurodevelopmental features is poorly understood. Mining single cell data from cerebral organoids and human fetal cortices, we found that NEUROG2 expression is enriched in basal neural progenitor cells. To identify and purify NEUROG2-expressing cells and trace their short-term lineage, we engineered two NEUROG2-mCherry knock-in human embryonic stem cell lines to produce cerebral organoids. Transcriptomic profiling of mCherry-high organoid cells revealed elevated expression of PPP1R17, associated with a fast-evolving human-accelerated regulatory region, oligodendrocyte precursor cell and extracellular matrix-associated gene transcripts. Conversely, only neurogenic gene transcripts were enriched in mCherry-high cortical cells from Neurog2:mCherry knock-in mice. Finally, we show that Neurog2 is sufficient to induce Ppp1r17, which slows human neural progenitor cell division, and Col13a1, an extracellular matrix gene, in P19 cells. NEUROG2 thus regulates a human neurodevelopmental gene regulatory program implicated in supporting a pro-proliferative basal progenitor cell niche and tempering the neurogenic pace.

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Section: Introductionmentioning

confidence: 99%

NEUROG2regulates a human-specific neurodevelopmental gene regulatory program

Chinchalongporn,

Vasan,

Saleh

et al. 2024

Preprint

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Early life stress, literacy and dyslexia: an evolutionary perspective

Kershner

2024

Brain Struct Funct

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Stress and learning co-evolved in parallel, with their interdependence critical to the survival of the species. Even today, the regulation of moderate levels of stress by the central autonomic network (CAN), especially during pre- and post-natal periods, facilitates biological adaptability and is an essential precursor for the cognitive requisites of learning to read. Reading is a remarkable evolutionary achievement of the human brain, mysteriously unusual, because it is not pre-wired with a genetic address to facilitate its acquisition. There is no gene for reading. The review suggests that reading co-opts a brain circuit centered in the left hemisphere ventral occipital cortex that evolved as a domain-general visual processor. Its adoption by reading depends on the CAN’s coordination of the learning and emotional requirements of learning to read at the metabolic, cellular, synaptic, and network levels. By stabilizing a child’s self-control and modulating the attention network’s inhibitory controls over the reading circuit, the CAN plays a key role in school readiness and learning to read. In addition, the review revealed two beneficial CAN evolutionary adjustments to early-life stress “overloads” that come with incidental costs of school under-performance and dyslexia. A short-term adaptation involving methylation of the FKBP5 and NR3C1 genes is a liability for academic achievement in primary school. The adaptation leading to dyslexia induces alterations in BDNF trafficking, promoting long-term adaptive fitness by protecting against excessive glucocorticoid toxicity but risks reading difficulties by disruptive signaling from the CAN to the attention networks and the reading circuit.

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Epigenetic control and manipulation of neuronal maturation timing

Ciceri,

Studer

2024

Current Opinion in Genetics & Development

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Human neuronal maturation comes of age: cellular mechanisms and species differences

Cited by 3 publications

References 273 publications

NEUROG2regulates a human-specific neurodevelopmental gene regulatory program

NEUROG2regulates a human-specific neurodevelopmental gene regulatory program

Early life stress, literacy and dyslexia: an evolutionary perspective

Epigenetic control and manipulation of neuronal maturation timing

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