Diverse Roles for MAPK Signaling in Circadian Clocks

Goldsmith, Charles S.; Bell-Pedersen, Deborah

doi:10.1016/b978-0-12-407703-4.00001-3

Cited by 85 publications

(66 citation statements)

References 130 publications

(261 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Together, these data indicated that ADV-1 functions within a circadian output pathway, potentially controlling rhythmicity for both direct and indirect gene targets involved in development, environmental sensing, metabolism, and cell fusion. Clock control of development, environmental sensing, and metabolism are well established (Brown 2014; Summa and Turek 2014; Goldsmith and Bell-Pedersen 2013; Bass and Takahashi 2010). However, the data indicating that the clock regulates aspects of cell fusion were unexpected.…”

Section: Resultsmentioning

confidence: 99%

TheNeurosporaTranscription Factor ADV-1 Transduces Light Signals and Temporal Information to Control Rhythmic Expression of Genes Involved in Cell Fusion

Dekhang

Smith

et al. 2017

G3 Genes|Genomes|Genetics

Self Cite

View full text Add to dashboard Cite

Light and the circadian clock have a profound effect on the biology of organisms through the regulation of large sets of genes. Toward understanding how light and the circadian clock regulate gene expression, we used genome-wide approaches to identify the direct and indirect targets of the light-responsive and clock-controlled transcription factor ADV-1 in Neurospora crassa. A large proportion of ADV-1 targets were found to be light- and/or clock-controlled, and enriched for genes involved in development, metabolism, cell growth, and cell fusion. We show that ADV-1 is necessary for transducing light and/or temporal information to its immediate downstream targets, including controlling rhythms in genes critical to somatic cell fusion. However, while ADV-1 targets are altered in predictable ways in Δadv-1 cells in response to light, this is not always the case for rhythmic target gene expression. These data suggest that a complex regulatory network downstream of ADV-1 functions to generate distinct temporal dynamics of target gene expression relative to the central clock mechanism.

show abstract

Section: Resultsmentioning

confidence: 99%

TheNeurosporaTranscription Factor ADV-1 Transduces Light Signals and Temporal Information to Control Rhythmic Expression of Genes Involved in Cell Fusion

Dekhang

Smith

et al. 2017

G3 Genes|Genomes|Genetics

Self Cite

View full text Add to dashboard Cite

show abstract

“…Clock genes are all transcription factors regulated by epigenetic and kinase modulators [252627]. Therefore, we decided to test compounds affecting these pathways on the expression of clock genes in differentiated P19 cells.…”

Section: Resultsmentioning

confidence: 99%

“…Kinases, such as those in the mitogen-activated protein kinase (MAPK) pathways, can function as inputs, allowing the endogenous clock to entrain to a 24-hour environmental cycle. MAPK pathways can also interact physically and/or genetically with components of the molecular circadian oscillator, implying that MAPK pathways can affect the cycling of the clock [27]. …”

Section: Discussionmentioning

confidence: 99%

P19 Cells as a Model for Studying the Circadian Clock in Stem Cells before and after Cell Differentiation

Mashhour¹,

Mansour²,

Hallaj³

et al. 2018

J Circadian Rhythms

View full text Add to dashboard Cite

In mammals, circadian rhythmicity is sustained via a transcriptional/translational feedback loop referred to as the canonical molecular circadian clock. Circadian rhythm is absent in undifferentiated embryonic stem cells; it begins only after differentiation. We used pluripotent P19 embryonal carcinoma stem cells to check the biological clock before and after differentiation into neurons using retinoic acid. We show that the central clock genes ARNTL (Bmal), Per2 and Per3, and the peripheral clock genes Rev-erb-α and ROR-α, oscillate before and after differentiation, as does the expression of the neuronal differentiation markers Hes5, β-3-tubulin (Tubb3) and Stra13, but not Neurod1. Furthermore, the known clock-modulating compounds ERK, EGFR, Pi3K, p38, DNA methylation and Sirtiun inhibitors, in addition to Rev-erb-α ligands, modulate the expression of central and peripheral clock genes. Interestingly Sirtinol, Sirt1 and Sirt2 inhibitors had the greatest significant effect on the expression of clock genes, and increased Hes5 and Tubb3 expression during neuronal differentiation. Our findings reveal a new frontier of circadian clock research in stem cells: contrary to what has been published previously, we have shown the clock to be functional and to oscillate, even in undifferentiated stem cells. Modulating the expression of clock genes using small molecules could affect stem cell differentiation.

show abstract

“…Three families of MAPK pathways, namely ERK, JNK and p38 have been understood [31]. We have known activation any of the three pathways (ERK, JNK and p38MAPK) is harmful, while suppression of any of the three MAPK pathways (ERK, JNK and p38MAPK) can alleviate the injury, is therefore protective [30,32]. Our date showed that OGD3h/R24 treatment significantly upregulated expression of all the three pathways, namely ERK, p38, and JNK, whereas the administration of NSP significantly, reversed this upregulation (Fig.…”

Section: Discussionmentioning

confidence: 99%

Neuroserpin Protects Rat Neurons and Microglia-Mediated Inflammatory Response Against Oxygen-Glucose Deprivation- and Reoxygenation Treatments in an In Vitro Study

Yang

Asakawa

Sha

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Neuroserpin (NSP) is known for its neuroprotective role in cerebral ischemic animal models and patients. Our laboratory conducted a series of investigations on the neuroprotection of NSP in different cells in the brain. In the present study, we further observe the effects of NSP on neurons and microglia-mediated inflammatory response following oxygen-glucose deprivation (OGD), and explore possible mechanisms related to neuroprotection of OGD in the central nervous system (CNS). Methods: Neurons and microglia from neonatal rats were treated with OGD followed by reoxygenation (OGD/R). To confirm the effects of NSP, the neuronal survival, neuronal apoptosis, and lactate dehydrogenase (LDH) release were measured in cultured neurons. Furthermore, the levels of IL-1β and nitric oxide (NO) release were also detected in cultured microglia. The possible mechanisms for the neuroprotective effect of NSP were explored using Western blot analysis. Results: NSP administration can reverse abnormal variations in neurons and microglia-mediated inflammatory response induced by OGD/R processes. The neuronal survival rate, neuronal apoptosis rate, and LDH release were significantly improved by NSP administration in neurons. Simultaneously, the release of IL-1β and NO were significantly reduced by NSP in microglia. Western blot showed that the expression of ERK, P38, and JNK was upregulated in microglia by the OGD/R treatment, and these effects were significantly inhibited by NSP. Conclusion: These data verified the neuroprotective effects of NSP on neurons and microglia-mediated inflammatory response. Inhibition of the mitogen-activated protein kinase (MAPK) signaling pathways might play a potential role in NSP neuroprotection on microglia-mediated inflammatory response, which needs further verification.

show abstract

Diverse Roles for MAPK Signaling in Circadian Clocks

Cited by 85 publications

References 130 publications

TheNeurosporaTranscription Factor ADV-1 Transduces Light Signals and Temporal Information to Control Rhythmic Expression of Genes Involved in Cell Fusion

TheNeurosporaTranscription Factor ADV-1 Transduces Light Signals and Temporal Information to Control Rhythmic Expression of Genes Involved in Cell Fusion

P19 Cells as a Model for Studying the Circadian Clock in Stem Cells before and after Cell Differentiation

Neuroserpin Protects Rat Neurons and Microglia-Mediated Inflammatory Response Against Oxygen-Glucose Deprivation- and Reoxygenation Treatments in an In Vitro Study

Contact Info

Product

Resources

About