The glucose-sensing transcription factor MLX promotes myogenesis via myokine signaling

Hunt, Liam C.; Xu, Beisi; Finkelstein, David; Fan, Yiping; Carroll, Patrick A.; Cheng, Pei-Feng; Eisenman, Robert N.; Demontis, Fabio

doi:10.1101/gad.267419.115

Cited by 45 publications

(39 citation statements)

References 65 publications

(68 reference statements)

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“…This is consistent with a report that MLX is responsive to, and suppresses, golgi stress in mammalian cell culture [110]. In addition, MLX null mice fail to regenerate muscle, compared to the rapid recovery of wildtype mice, following damage due to cardiotoxin treatment [111]. Furthermore, normal physiologic processes entailing high metabolic demand, such as T cell activation and spermatogenesis, are impaired in the absence of MLX (P.A.C.…”

Section: Involvement Of Mlxip-mlx In the Response To Cellular Stresssupporting

confidence: 91%

The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis

et al. 2018

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Transcription factor networks have evolved in order to control, coordinate, and separate, the functions of distinct network modules spatially and temporally. In this review we focus on the MYC network (also known as the MAX-MLX Network), a highly conserved super-family of related basic-helix-loop-helix-zipper (bHLHZ) proteins that functions to integrate extracellular and intracellular signals and modulate global gene expression. Importantly the MYC network has been shown to be deeply involved in a broad spectrum of human and other animal cancers. Here we summarize molecular and biological properties of the network modules with emphasis on functional interactions among network members. We suggest that these network interactions serve to modulate growth and metabolism at the transcriptional level in order to balance nutrient demand with supply, to maintain growth homeostasis, and to influence cell fate. Moreover, oncogenic activation of MYC and/or loss of a MYC antagonist, results in an imbalance in the activity of the network as a whole, leading to tumor initiation, progression and maintenance.

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Section: Involvement Of Mlxip-mlx In the Response To Cellular Stresssupporting

confidence: 91%

The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis

et al. 2018

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“…Western blots for monitoring Timeless protein levels were done according to standard procedures (Hunt et al 2015) by using anti-TIM (Garbe et al 2013;Jang et al 2015) and anti-tubulin antibodies (Cell Signaling Technologies, #2125). The band corresponding to Timeless protein (∼150 kDa) was confirmed to be specific via the analysis of positive controls (Supplemental Fig.…”

Section: Western Blottingmentioning

confidence: 99%

Circadian gene variants and the skeletal muscle circadian clock contribute to the evolutionary divergence in longevity across Drosophila populations

et al. 2019

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Organisms use endogenous clocks to adapt to the rhythmicity of the environment and to synchronize social activities. Although the circadian cycle is implicated in aging, it is unknown whether natural variation in its function contributes to differences in lifespan between populations and whether the circadian clock of specific tissues is key for longevity. We have sequenced the genomes of Drosophila melanogaster strains with exceptional longevity that were obtained via multiple rounds of selection from a parental strain. Comparison of genomic, transcriptomic, and proteomic data revealed that changes in gene expression due to intergenic polymorphisms are associated with longevity and preservation of skeletal muscle function with aging in these strains. Analysis of transcription factors differentially modulated in long-lived versus parental strains indicates a possible role of circadian clock core components. Specifically, there is higher period and timeless and lower cycle expression in the muscle of strains with delayed aging compared to the parental strain. These changes in the levels of circadian clock transcription factors lead to changes in the muscle circadian transcriptome, which includes genes involved in metabolism, proteolysis, and xenobiotic detoxification. Moreover, a skeletal muscle-specific increase in timeless expression extends lifespan and recapitulates some of the transcriptional and circadian changes that differentiate the long-lived from the parental strains. Altogether, these findings indicate that the muscle circadian clock is important for longevity and that circadian gene variants contribute to the evolutionary divergence in longevity across populations.

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“…), as well as CHORE motifs, which bind the glucose‐responsive transcription factor, MLX (Hunt et al . ). Therefore, the availability of oxygen and nutrients in utero could have direct effects on placental Igf2 .…”

Section: Introductionmentioning

confidence: 97%

Placental phenotype and the insulin‐like growth factors: resource allocation to fetal growth

Sferruzzi‐Perri

Sandovici²,

Constância³

et al. 2017

The Journal of Physiology

132

117

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The placenta is the main determinant of fetal growth and development in utero. It supplies all the nutrients and oxygen required for fetal growth and secretes hormones that facilitate maternal allocation of nutrients to the fetus. Furthermore, the placenta responds to nutritional and metabolic signals in the mother by altering its structural and functional phenotype, which can lead to changes in maternal resource allocation to the fetus. The molecular mechanisms by which the placenta senses and responds to environmental cues are poorly understood. This review discusses the role of the insulin-like growth factors (IGFs) in controlling placental resource allocation to fetal growth, particularly in response to adverse gestational environments. In particular, it assesses the impact of the IGFs and their signalling machinery on placental morphogenesis, substrate transport and hormone secretion, primarily in the laboratory species, although it draws on data from human and other species where relevant. It also considers the role of the IGFs as environmental signals in linking resource availability to fetal growth through changes in the morphological and functional phenotype of the placenta. As altered fetal growth is associated with increased perinatal morbidity and mortality and a greater risk of developing adult-onset diseases in later life, understanding the role of IGFs during pregnancy in regulating placental resource allocation to fetal growth is important for identifying the mechanisms underlying the developmental programming of offspring phenotype by suboptimal intrauterine growth.

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The glucose-sensing transcription factor MLX promotes myogenesis via myokine signaling

Cited by 45 publications

References 65 publications

The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis

The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis

Circadian gene variants and the skeletal muscle circadian clock contribute to the evolutionary divergence in longevity across Drosophila populations

Placental phenotype and the insulin‐like growth factors: resource allocation to fetal growth

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