RUNX1T1 function in cell fate

Hu, Nan; Zou, Lin; Wang, Cheng; Song, Guoqi

doi:10.1186/s13287-022-03074-w

Cited by 9 publications

(9 citation statements)

References 64 publications

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“…6D). While ChIP-seq binding data does not indicate whether these interactions are activatory or repressive, BCOR (binds 98.6% of cluster 2 genes) and RUNX1T1 (binds 95.1% of cluster 2 genes) are both known repressors 73–75 . NEUROD1 (binds 94.6% of cluster 2 genes) however, is more complicated since it has been shown to act as an activator as well as repressor 76 , but it is possible that the I1-FFL motif is formed by the combined interactions of the target genes.…”

Section: Resultsmentioning

confidence: 97%

NGN3 oscillatory expression controls the timing of human pancreatic endocrine differentiation

Miller,

Biga,

Rowntree

et al. 2024

Preprint

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SummaryUnderstanding protein expression dynamics is crucial for the mechanistic understanding of cell differentiation. We investigate the dynamics of NGN3, a transcription factor critical for pancreatic endocrine development, including their function and decoding mechanisms. A knock-in endogenous reporter shows that the expression of NGN3 protein oscillates with a 13-hour periodicity in human iPS-derived endocrine progenitors and is switched off as cells differentiate to β-like and α-like cells. Increasing the stability of NGN3 protein results in one broad peak of expression instead of oscillations, with a larger peak to trough fold-change. This leads to precocious endocrine differentiation to both β-like and α-like cells and precocious expression of key NGN3 target genes. Single-cell analysis of dynamics, mathematical modelling and bioinformatics suggest that decoding of NGN3 oscillations occurs by fold-change detection via an incoherent feedforward motif that explains both normal and precocious differentiation. Our findings suggest that oscillatory NGN3 dynamics control the timing of differentiation, but not fate specification.

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Section: Resultsmentioning

confidence: 97%

NGN3 oscillatory expression controls the timing of human pancreatic endocrine differentiation

Miller,

Biga,

Rowntree

et al. 2024

Preprint

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“…Skeletal muscle development, as known as myogenesis, is a complex multistep process and its underling molecular mechanism are not yet fully understood. RUNX1T1 has been shown to play an important role in cellular development, including cell proliferation and differentiation 33,34 . However, its role in regulating myogenesis and the underlying mechanisms remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…RUNX1T1 has been shown to play an important role in cellular development, including cell proliferation and differentiation. 33,34 However, its role in regulating myogenesis and the underlying mechanisms remain unclear. In this study, we observed that goat RUX1T1 CDS sequence is highly homologous to that of ovine and both can encode 602 amino acids, 24 which is different from that of cattle and mice.…”

Section: Discussionmentioning

confidence: 99%

RUNX1T1 modulates myogenic differentiation by regulating the calcium signaling pathway and the alternative splicing of ROCK2

Deng

Liu

et al. 2023

The FASEB Journal

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RUNX1T1 (Runt-related transcription factor 1, translocated to 1) plays a wideranging and diverse role in cellular development, including hematopoiesis and adipogenesis. However, little is known about the function of RUNX1T1 in the skeletal muscle development. Here, we assessed the impact of RUNX1T1 on the proliferation and myogenic differentiation of goat primary myoblasts (GPMs). It was observed that RUNX1T1 is highly expressed during the early stages of myogenic differentiation and the fetal stage. Moreover, the knockdown of RUNX1T1 promotes the proliferation and inhibits myogenic differentiation and mitochondrial biogenesis of GPMs. RNA sequencing analysis revealed that significantly differentially expressed genes in RUNX1T1 knockdown cells were enriched in the calcium signaling pathway. Additionally, we discovered that RUNX1T1 regulates alternative splicing (AS) events involved in myogenesis. We also show that silencing RUNX1T1 blocked the Ca 2+ -CAMK signaling pathway and reduced the expression levels of muscle-specific isoforms of recombinant rho associated coiled coil containing crotein kinase 2 (ROCK2) during myogenic differentiation, partially explaining why RUNX1T1 deficiency leads to the impairment of myotube formation. These findings suggest that RUNX1T1 is a novel regulator of myogenic differentiation that regulates the calcium signaling pathway and AS of ROCK2. Overall, our results highlight the critical role of RUNX1T1 in myogenesis and broaden our understanding of myogenic differentiation.

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“…The last evidence showed that the adipogenesis induced by ZFP217 knockdown was caused by CCND1, which was mediated by METTL3 and YTHDF2 in an m 6 A-dependent manner [ 115 ]. Runt-related transcription factor 1 translocation partner 1 (RUNX1T1) is another novel adipogenic regulatory factor [ 116 ]. By modulating the amounts of m 6 A around splice sites, FTO regulates the exonic splicing of RUNX1T1, controlling RUNX1T1-S isoform expression and therefore modulating adipogenesis [ 117 ].…”

Section: A Modification and Adipogenesis Of Bmscsmentioning

confidence: 99%

N6-Methyladenosine in Cell-Fate Determination of BMSCs: From Mechanism to Applications

Zhang,

Li,

Wang

et al. 2024

Research

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The methylation of adenosine base at the nitrogen-6 position is referred to as “N6-methyladenosine (m 6 A)” and is one of the most prevalent epigenetic modifications in eukaryotic mRNA and noncoding RNA (ncRNA). Various m 6 A complex components known as “writers,” “erasers,” and “readers” are involved in the function of m 6 A. Numerous studies have demonstrated that m 6 A plays a crucial role in facilitating communication between different cell types, hence influencing the progression of diverse physiological and pathological phenomena. In recent years, a multitude of functions and molecular pathways linked to m 6 A have been identified in the osteogenic, adipogenic, and chondrogenic differentiation of bone mesenchymal stem cells (BMSCs). Nevertheless, a comprehensive summary of these findings has yet to be provided. In this review, we primarily examined the m 6 A alteration of transcripts associated with transcription factors (TFs), as well as other crucial genes and pathways that are involved in the differentiation of BMSCs. Meanwhile, the mutual interactive network between m 6 A modification, miRNAs, and lncRNAs was intensively elucidated. In the last section, given the beneficial effect of m 6 A modification in osteogenesis and chondrogenesis of BMSCs, we expounded upon the potential utility of m 6 A-related therapeutic interventions in the identification and management of human musculoskeletal disorders manifesting bone and cartilage destruction, such as osteoporosis, osteomyelitis, osteoarthritis, and bone defect.

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RUNX1T1 function in cell fate

Cited by 9 publications

References 64 publications

NGN3 oscillatory expression controls the timing of human pancreatic endocrine differentiation

NGN3 oscillatory expression controls the timing of human pancreatic endocrine differentiation

RUNX1T1 modulates myogenic differentiation by regulating the calcium signaling pathway and the alternative splicing of ROCK2

N6-Methyladenosine in Cell-Fate Determination of BMSCs: From Mechanism to Applications

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