All in the family: proneural bHLH genes and neuronal diversity

Baker, Nicholas E.; Brown, Nadean L.

doi:10.1242/dev.159426

Cited by 72 publications

(63 citation statements)

References 103 publications

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“…Immunostaining of E14 retinas confirm a reduction in the number of cells 582 immunopositive for Brn3a (Pou4f1) and Brn3b (Pou4f2) ( Figure 4J), as well as the pan-583 RGC markers RBPMS and Isl1 ( Figure 4K and Brown, 2018). In this study, though, we show that specification of the great majority 652 of RGCs occurs normally even in the absence of Atoh7.…”

Section: Rgc Differentiation Is Delayed In the Absence Of Atoh7 512mentioning

confidence: 58%

Atoh7-independent specification of retinal ganglion cell identity

Brodie-Kommit

Hattar

Clark³

et al. 2020

Preprint

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36Retinal ganglion cells (RGCs), which relay visual information from the eye to the brain, 37 are the first cell type generated during retinal neurogenesis. Loss of function of the 38 transcription factor Atoh7, which is expressed in multipotent early neurogenic retinal 39 progenitor cells, leads to a selective and near complete loss of RGCs. Atoh7 has thus 40 been considered essential for conferring competence on progenitors to generate RGCs. 41However, when apoptosis is inhibited in Atoh7-deficient mice by loss of function of Bax, 42 only a modest reduction in RGC number is observed. Single-cell RNA-Seq of 43Atoh7;Bax-deficient retinas shows that RGC differentiation is delayed, but that RGC 44 precursors are grossly normal. Atoh7;Bax-deficient RGCs eventually mature, fire action 45 potentials, and incorporate into retinal circuitry, but exhibit severe axonal guidance 46 defects. This study reveals an essential role for Atoh7 in RGC survival, and 47

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Section: Rgc Differentiation Is Delayed In the Absence Of Atoh7 512mentioning

confidence: 58%

Atoh7-independent specification of retinal ganglion cell identity

Brodie-Kommit

Hattar

Clark³

et al. 2020

Preprint

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“…The bHLH proteins promote neurogenesis by inducing changes in the gene expression required for neuronal differentiation [11,12,23], including the MTG genes. The MTG family is a small group of transcriptional repressors, which bridges various transcription factors severed as "protein scaffolds."…”

Section: Discussionmentioning

confidence: 99%

“…Neurogenesis in the dentate gyrus (DG) of hippocampus can persist throughout the whole life [5][6][7][8], and it is also a multiple-step process and is regulated by several intrinsic and extrinsic factors [9,10]. During the neurogenesis, a cascade of gene expression activated by proneural basic helix-loop-helix (bHLH) proteins plays an essential and conserved role in promoting neuronal differentiation [11,12], such as myeloid translocation genes (MTGs). MTG proteins have been reported to be sequentially expressed during neuronal differentiation and may promote the transition from precursor to neuron and induce the expression of neuronal genes in the differentiated cells [13].…”

Section: Introductionmentioning

confidence: 99%

Runx1t1 promotes the neuronal differentiation in rat hippocampus

Zou

Han

et al. 2020

Stem Cell Res Ther

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Background: Runt-related transcription factor 1 translocated to 1 (Runx1t1) is one of the members of the myeloid translocation gene family. Our previous work showed that Runx1t1 induced the neuronal differentiation of radial glia cells in vitro. Methods: To better uncover the role of Runx1t1 in hippocampal neurogenesis, in this study, we further explore its localization and function during the hippocampal neurogenesis. Results: Our results showed that insufficient expression of Runx1t1 reduced the neuronal differentiation, and overexpression of Runx1t1 promoted the neuronal differentiation in vitro. We also found that Runx1t1 localized in neurons but not astrocytes both in vivo and in vitro. Furthermore, we found that Runx1t1 overexpression elevated the number of newborn neurons in the hippocampal dentate gyrus. Conclusions: Taken together, our results further proved that Runx1t1 could be worked as a regulator in the process of hippocampal neurogenesis.

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“…These events are governed (in part) by transcription factors that regulate expression of genes involved in the cell cycle and neuronal differentiation. The basic-loop-helix (bHLH) transcription factors play prominent roles in these events (Akagi et al, 2004; Baker & Brown, 2018; Joseph A. Brzezinski, Kim, Johnson, & Reh, 2011; Mao et al, 2013; Ohsawa & Kageyama, 2008; Pollak et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

The microRNA, miR-18a, regulates NeuroD and photoreceptor differentiation in the retina of the zebrafish

Taylor

Giuffre

Moseley

et al. 2018

Preprint

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During embryonic retinal development, six types of retinal neurons are generated from a pool of multipotent progenitors in a strict spatiotemporal pattern. This pattern requires cell cycle exit (i.e. neurogenesis) and differentiation to be precisely regulated in a lineage-specific manner. In zebrafish, the bHLH transcription factor NeuroD governs photoreceptor genesis through Notch signaling but also governs photoreceptor differentiation though distinct mechanisms that are currently unknown. Also unknown are the mechanisms that regulate NeuroD and the spatiotemporal pattern of photoreceptor development. Members of the miR-17-92 microRNA cluster regulate CNS neurogenesis, and a member of this cluster, miR-18a, is predicted to target neuroD mRNA. The purpose of this study was to determine if miR-18a regulates NeuroD in the retina and if it plays a role in photoreceptor development. Quantitative RT-PCR showed that, of the three miR-18 family members (miR-18a, b and c), miR-18a expression most closely parallels neuroD expression. Morpholino oligonucleotides and CRISPR/Cas9 gene editing were used for miR-18a loss-of-function (LOF) and both approaches resulted in larvae with more mature photoreceptors at 70 hpf without affecting cell proliferation. Western blot showed that miR-18a LOF increases NeuroD protein levels and in vitro dual luciferase assay showed that miR-18a directly interacts with the 32UTR of neuroD. Finally, tgif1 mutants have increased miR-18a expression, less NeuroD protein and fewer mature photoreceptors, and the photoreceptor deficiency is rescued by miR-18a knockdown. Together these results show that, independent of neurogenesis, miR-18a regulates the timing of photoreceptor differentiation and indicate that this occurs through post-transcriptional regulation of NeuroD.

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All in the family: proneural bHLH genes and neuronal diversity

Cited by 72 publications

References 103 publications

Atoh7-independent specification of retinal ganglion cell identity

Atoh7-independent specification of retinal ganglion cell identity

Runx1t1 promotes the neuronal differentiation in rat hippocampus

The microRNA, miR-18a, regulates NeuroD and photoreceptor differentiation in the retina of the zebrafish

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