A C. elegans Myc-like network cooperates with semaphorin and Wnt signaling pathways to control cell migration

Pickett, Christopher L.; Breen, Kevin T.; Ayer, Donald E.

doi:10.1016/j.ydbio.2007.07.034

Cited by 41 publications

(60 citation statements)

References 80 publications

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“…For example, C. elegans mep-1/Kruppel-like represses germline transcription in somatic cells, indicating that Kruppel-like factors promote a somatic or differentiated state in C. elegans (Unhavaithaya et al, 2002). mml-1 is homologous to vertebrate c-myc , but mml-1 mutants have no known embryonic phenotype (Pickett et al, 2007). …”

Section: Discussionmentioning

confidence: 99%

The Polycomb Complex Protein mes-2/E(z) Promotes the Transition from Developmental Plasticity to Differentiation in C. elegans Embryos

et al. 2009

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SUMMARY We have used expression profiling and in vivo imaging to characterize C. elegans embryos as they transit from a developmentally plastic state to the onset of differentiation. Normally, this transition is accompanied by activation of developmental regulators and differentiation genes, down-regulation of early-expressed genes, and large-scale re-organization of chromatin. We find that loss of plasticity and differentiation onset depends on the Polycomb complex protein mes-2/E(Z). mes-2 mutants display prolonged developmental plasticity in response to heterologous developmental regulators. Early-expressed genes remain active, differentiation genes fail to reach wild-type levels, and chromatin retains a decompacted morphology in mes-2 mutants. By contrast, loss of developmental regulators pha-4/FoxA or end-1/GATA does not prolong plasticity. This study establishes a model to analyze developmental plasticity within an intact embryo. mes-2 orchestrates large-scale changes in chromatin organization and gene expression to promote the timely loss of developmental plasticity. Our findings indicate that loss of plasticity can be uncoupled from cell fate specification.

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Section: Discussionmentioning

confidence: 99%

The Polycomb Complex Protein mes-2/E(z) Promotes the Transition from Developmental Plasticity to Differentiation in C. elegans Embryos

et al. 2009

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“…Nematodes show extensive divergence, presumably owing to a massive gene reduction and rearrangement (Witherspoon and Robertson 2003;Denver et al 2004;Coghlan 2005), and contain two MAX orthologs (Mxl-1 and Mxl-3), a single MLX ortholog (Mxl-2), a MXD-like protein (MDL-1), and a MYC and Mondo-like protein (MML-1). Mxl-1 and Mxl-3 apparently heterodimerize with MDL-1, whereas Mxl-2 binds MML-1 (Yuan et al 1998;Gallant 2006;Pickett et al 2007). Hence, the MLX network is conserved in nematodes, but it is not known if the antagonistic transcriptional regulation characteristic of MYC and MNT is performed by MDL-1 and MML-1.…”

Section: Network Divergencementioning

confidence: 99%

An Overview of MYC and Its Interactome

Conacci‐Sorrell

McFerrin

Eisenman

2014

Cold Spring Harbor Perspectives in Medicine

336

398

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This review is intended to provide a broad outline of the biological and molecular functions of MYC as well as of the larger protein network within which MYC operates. We present a view of MYC as a sensor that integrates multiple cellular signals to mediate a broad transcriptional response controlling many aspects of cell behavior. We also describe the larger transcriptional network linked to MYC with emphasis on the MXD family of MYC antagonists. Last, we discuss evidence that the network has evolved for millions of years, dating back to the emergence of animals.

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“…Luciferase reporter assays, immunofluorescence, and microscopy were conducted in HA1ER and A549 cells as previously described (7,29).…”

Section: Preparation Of 45-dioxo-5-[3-(trifluoromethyl)benzyloxy]penmentioning

confidence: 99%

Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity

Kaadige

Looper

Kamalanaadhan

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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143

187

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Glucose and glutamine are abundant nutrients required for cell growth, yet how cells sense and adapt to changes in their levels is not well understood. The MondoA transcription factor forms a heterocomplex with its obligate partner Mlx to regulate Ϸ75% of glucose-dependent transcription. By mediating glucose-induced activation of thioredoxin-interacting protein (TXNIP), MondoA:Mlx complexes directly repress glucose uptake. We show here that glutamine inhibits transcriptional activation of TXNIP by triggering the recruitment of a histone deacetylase-dependent corepressor to the amino terminus of MondoA. Therefore, in the presence of both glucose and glutamine, TXNIP expression is low, which favors glucose uptake and aerobic glycolysis; the Warburg effect. Consistent with MondoA functioning upstream of TXNIP, MondoA knockdown reduces TXNIP expression, elevates glucose uptake and stimulates cell proliferation. Although glutamine has many intracellular fates, a cell permeable analog of a tricarboxylic acid cycle (TCA) intermediate, ␣-ketoglutarate, also blocks the transcriptional activity of MondoA at the TXNIP promoter and stimulates glucose uptake. Together our data suggest that glutaminedependent mitochondrial anapleurosis dictates glucose uptake and aerobic glycolysis by blocking MondoA:Mlx-dependent transcriptional activation of TXNIP. We propose that this previously unappreciated coordination between glutamine and glucose utilization defines a metabolic checkpoint that restricts cell growth when subthreshold levels of these essential nutrients are available.metabolism ͉ mitochondria ͉ transcription ͉ bHLHZIP

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A C. elegans Myc-like network cooperates with semaphorin and Wnt signaling pathways to control cell migration

Cited by 41 publications

References 80 publications

The Polycomb Complex Protein mes-2/E(z) Promotes the Transition from Developmental Plasticity to Differentiation in C. elegans Embryos

The Polycomb Complex Protein mes-2/E(z) Promotes the Transition from Developmental Plasticity to Differentiation in C. elegans Embryos

An Overview of MYC and Its Interactome

Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity

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