scholarly journals Gene array analysis of neural crest cells identifies transcription factors necessary for direct conversion of embryonic fibroblasts into neural crest cells

Biology Open ◽  
2016 ◽  
Vol 5 (3) ◽  
pp. 311-322 ◽  
Author(s):  
Tsutomu Motohashi ◽  
Natsuki Watanabe ◽  
Masahiro Nishioka ◽  
Yuhki Nakatake ◽  
Piao Yulan ◽  
...  
2001 ◽  
Vol 75 (20) ◽  
pp. 9909-9917 ◽  
Author(s):  
Dimitra Tsavachidou ◽  
Wawrzyniec Podrzucki ◽  
John Seykora ◽  
Shelley L. Berger

ABSTRACT The earliest events within the peripheral mammalian nervous system that cause herpes simplex virus type 1 (HSV-1) to reactivate from latency are unknown but are highly likely to include altered regulation of cellular transcription factors. Using gene array analysis, we have examined the changes that occur in cellular mRNA levels in mouse trigeminal ganglia following explantation, a stimulus that results in HSV-1 reactivation from latency. We have detected both increased and decreased expression levels of particular cellular transcripts, which include RNAs encoding neuronal factors, transcription factors, and factors involved in the cell cycle. Among the transcription factors that are upregulated is Bcl-3, a coactivator for NFκB. We have confirmed these increases in Bcl-3 transcription levels using reverse transcription-PCR and S1 nuclease protection assays. In addition, we have shown Bcl-3 upregulation at the protein level. Importantly, Bcl-3 RNA levels were found to increase specifically in neuronal cells within the trigeminal ganglia. We discuss a potential role for this factor in upregulating ICP0 transcription, which is an important viral event for initiation of HSV-1 reactivation.


Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1467-1479 ◽  
Author(s):  
R. Kos ◽  
M.V. Reedy ◽  
R.L. Johnson ◽  
C.A. Erickson

The winged-helix or forkhead class of transcription factors has been shown to play important roles in cell specification and lineage segregation. We have cloned the chicken homolog of FoxD3, a member of the winged-helix class of transcription factors, and analyzed its expression. Based on its expression in the dorsal neural tube and in all neural crest lineages except the late-emigrating melanoblasts, we predicted that FoxD3 might be important in the segregation of the neural crest lineage from the neural epithelium, and for repressing melanogenesis in early-migrating neural crest cells. Misexpression of FoxD3 by electroporation in the lateral neural epithelium early in neural crest development produced an expansion of HNK1 immunoreactivity throughout the neural epithelium, although these cells did not undergo an epithelial/mesenchymal transformation. To test whether FoxD3 represses melanogenesis in early migrating neural crest cells, we knocked down expression in cultured neural crest with antisense oligonucleotides and in vivo by treatment with morpholino antisense oligonucleotides. Both experimental approaches resulted in an expansion of the melanoblast lineage, probably at the expense of neuronal and glial lineages. Conversely, persistent expression of FoxD3 in late-migrating neural crest cells using RCAS viruses resulted in the failure of melanoblasts to develop. We suggest that FoxD3 plays two important roles in neural crest development. First, it is involved in the segregation of the neural crest lineage from the neuroepithelium. Second, it represses melanogenesis, thereby allowing other neural crest derivatives to differentiate during the early stages of neural crest patterning.


2020 ◽  
Vol 29 (23) ◽  
pp. 1510-1519
Author(s):  
Tsutomu Motohashi ◽  
Norito Kawamura ◽  
Natsuki Watanabe ◽  
Daisuke Kitagawa ◽  
Naoki Goshima ◽  
...  

2008 ◽  
Vol 3 ◽  
pp. BMI.S600 ◽  
Author(s):  
S. Chiosea ◽  
M. Acquafondata ◽  
J. Luo ◽  
SF. Kuan ◽  
RR. Seethala

Differential microRNA expression in colon adenocarcinoma (CA) was previously reported. MicroRNA biogenesis and function requires a set of proteins designated as the microRNA machinery, which includes DICER1 and PRKRA. Loss of heterozygosity at 14q32.13 DICER1 locus was detected in up to 60% of CA cases. The in silico gene array analysis of CA showed down-regulation of DICER1 and an up-regulation of PRKRA. Immunohistochemically, DICER1 expression was abnormal in 65% of CA (95 of 147 cases). PRKRA was deregulated in 70% of CA (32 of 46 cases). Expression of DICER1 and PRKRA was correlated with clinicopathologic features of CA. DICER1 up-regulation was seen more commonly in women. Only 10 of 46 cases immunostained for both DICER1 and PRKRA showed normal levels of both DICER1 and PRKRA. Microsatellite status of 32 cases was determined. Microsatellite instable cases showed DICER1 up-regulation more commonly when compared to microsatellite stable cases; however, this trend was not statistically significant. Abnormal DICER1 and/or PRKRA expression might explain the observed changes in microRNA profile. The status of the endogenous DICER1 and PRKRA in CA may help to predict the response to future RNA interference-based therapy.


2002 ◽  
Vol 942 (1-2) ◽  
pp. 120-123 ◽  
Author(s):  
Stacey A. Trotter ◽  
Louis B. Brill II ◽  
James P. Bennett

2001 ◽  
Vol 120 (5) ◽  
pp. A88
Author(s):  
Qingding Wang ◽  
Robert Thomas ◽  
Nan Li ◽  
Xiaofu Wang ◽  
B. Mark Evers

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