Extracellular signal regulation of cell differentiation in biofilms

MRS Bulletin ◽  
2011 ◽  
Vol 36 (5) ◽  
pp. 374-379 ◽  
Author(s):  
Liraz Chai ◽  
Hera Vlamakis ◽  
Roberto Kolter
Keyword(s):  
Cell Differentiation ◽  
Extracellular Signal ◽  
Image Position ◽  
Signal Regulation

Abstract

scholarly journals Retinoic Acid Induces Differentiation of Mouse F9 Embryonic Carcinoma Cell by Modulating the miR-485 Targeting of Abhd2

2019 ◽  
Vol 20 (9) ◽  
pp. 2071 ◽  
Author(s):  
Mengying Yu ◽  
Lei Zhang ◽  
Yingxiang Liu ◽  
Defu Liu ◽  
Zekun Guo
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Extracellular Signal Regulated Kinase ◽  
Embryonic Carcinoma ◽  
Extracellular Signal ◽  
Embryonic Carcinoma Cells ◽  
Embryonic Carcinoma Cell ◽  
Mediate Cell

Retinoic acid (RA) plays a key role in pluripotent cell differentiation. In F9 embryonic carcinoma cells, RA can induce differentiation towards somatic lineages via the Ras-extracellular signal-regulated kinase (Ras/Erk) pathway, but the mechanism through which it induces the Erk1/2 phosphorylation is unclear. Here, we show that miR-485 is a positive regulator that targets α/β-hydrolase domain-containing protein 2 (Abhd2), which can result in Erk1/2 phosphorylation and triggers differentiation. RA up-regulates miR-485 and concurrently down-regulates Abhd2. We verified that Abhd2 is targeted by miR-485 and they both can influence the phosphorylation of Erk1/2. In summary, RA can mediate cell differentiation by phosphorylating Erk1/2 via miR-485 and Abhd2.

scholarly journals Autophagy-associated alpha-arrestin signaling is required for conidiogenous cell development in Magnaporthe oryzae

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Bo Dong ◽  
Xiaojin Xu ◽  
Guoqing Chen ◽  
Dandan Zhang ◽  
Mingzhi Tang ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Magnaporthe Oryzae ◽  
Conidiogenous Cell ◽  
Blast Disease ◽  
Autophagic Flux ◽  
Distribution Profile ◽  
Extracellular Signal ◽  
Related Transcription Factor ◽  
Specific Receptors ◽  
Autophagosome Maturation

Abstract Conidiation patterning is evolutionarily complex and mechanism concerning conidiogenous cell differentiation remains largely unknown. Magnaporthe oryzae conidiates in a sympodial way and uses its conidia to infect host and disseminate blast disease. Arrestins are multifunctional proteins that modulate receptor down-regulation and scaffold components of intracellular trafficking routes. We here report an alpha-arrestin that regulates patterns of conidiation and contributes to pathogenicity in M. oryzae. We show that disruption of ARRDC1 generates mutants which produce conidia in an acropetal array and ARRDC1 significantly affects expression profile of CCA1, a virulence-related transcription factor required for conidiogenous cell differentiation. Although germ tubes normally develop appressoria, penetration peg formation is dramatically impaired and Δarrdc1 mutants are mostly nonpathogenic. Fluorescent analysis indicates that EGFP-ARRDC1 puncta are well colocalized with DsRed2-Atg8, and this distribution profile could not be altered in Δatg9 mutants, suggesting ARRDC1 enters into autophagic flux before autophagosome maturation. We propose that M. oryzae employs ARRDC1 to regulate specific receptors in response to conidiation-related signals for conidiogenous cell differentiation and utilize autophagosomes for desensitization of conidiogenous receptor, which transmits extracellular signal to the downstream elements of transcription factors. Our investigation extends novel significance of autophagy-associated alpha-arrestin signaling to fungal parasites.

The adaptor protein SH2D1A regulates signaling through CD150 (SLAM) in B cells

Blood ◽  
2004 ◽  
Vol 104 (13) ◽  
pp. 4063-4070 ◽  
Author(s):  
Svitlana V. Mikhalap ◽  
Larysa M. Shlapatska ◽  
Olga V. Yurchenko ◽  
Maria Y. Yurchenko ◽  
Ganna G. Berdova ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Adaptor Protein ◽  
Sh2 Domain ◽  
B Cell Differentiation ◽  
Akt Phosphorylation ◽  
Inositol Phosphatase ◽  
Extracellular Signal ◽  
Inositol Phosphatases

Abstract The CD150 receptor is expressed on activated T and B lymphocytes, dendritic cells, and monocytes. A TxYxxV/I motif in the CD150 cytoplasmic tail can bind different SH2-containing molecules, including tyrosine and inositol phosphatases, Src family kinases, and adaptor molecules. To analyze CD150-initiated signal transduction pathways, we used DT40 B-cell sublines deficient in these molecules. CD150 ligation on DT40 transfectants induced the extracellular signal-regulated kinase (ERK) pathway, which required SH2-containing inositol phosphatase (SHIP) but not SH2 domain protein 1A (SH2D1A). CD150-mediated Akt phosphorylation required Syk and SH2D1A, was negatively regulated by Lyn and Btk, but was SHIP independent. Lyn directly phosphorylated Y327 in CD150, but the Akt pathway did not depend on CD150 tyrosine phosphorylation and CD150-SHP-2 association. Analysis of CD150 and SH2D1A expression in non-Hodgkin and Hodgkin lymphomas revealed stages of B-cell differentiation where these molecules are expressed alone or coexpressed. Signaling studies in Hodgkin disease cell lines showed that CD150 is linked to the ERK and Akt pathways in neoplastic B cells. Our data support the hypothesis that CD150 and SH2D1A are coexpressed during a narrow window of B-cell maturation and SH2D1A may be involved in regulation of B-cell differentiation via switching of CD150-mediated signaling pathways. (Blood. 2004;104:4063-4070)

scholarly journals Extracellular signal-regulated kinase (ERK) pathway control of CD8+ T cell differentiation

2020 ◽  
Author(s):  
Marcos P Damasio ◽  
Julia M Marchingo ◽  
Laura Spinelli ◽  
Jens Hukelmann ◽  
Doreen Cantrell ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
T Cell Activation ◽  
Cd8 T Cells ◽  
Cell Activation ◽  
Antigen Receptor ◽  
T Cell Differentiation ◽  
Signalling Pathways ◽  
Extracellular Signal

The integration of multiple signalling pathways that co-ordinate T cell metabolism and transcriptional reprogramming is required to drive T cell differentiation and proliferation. One key T cell signalling module is mediated by extracellular signal-regulated kinases (ERKs) which are activated in response to antigen receptor engagement. The activity of ERKs is often used to report antigen receptor occupancy but the full details of how ERKs control T cell activation is not understood. Accordingly, we have used mass spectrometry to explore how ERK signalling pathways control antigen receptor driven proteome restructuring in CD8+ T cells to gain insights about the biological processes controlled by ERKs in primary lymphocytes. Quantitative analysis of >8000 proteins identified 900 ERK regulated proteins in activated CD8+ T cells. The data identify both positive and negative regulatory roles for ERKs during T cell activation and reveal that ERK signalling primarily controls the repertoire of transcription factors, cytokines and cytokine receptors expressed by activated T cells. It was striking that a large proportion of the proteome restructuring that is driven by triggering of the T cell antigen receptor is not dependent on ERK activation. However, the selective targets of the ERK signalling module include the critical effector molecules and the cytokines that allow T cell communication with other immune cells to mediate adaptive immune responses.

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