scholarly journals Src acts with WNT/FGFRL signaling to pattern the planarian anteroposterior axis

2021 ◽  
Author(s):  
Nicolle A. Bonar ◽  
David I. Gittin ◽  
Christian P. Petersen
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Posterior Pole ◽  
Control Gene ◽  
Downstream Signaling ◽  
Control Gene Expression ◽  
Signaling Mechanisms ◽  
Positional System ◽  
Canonical Wnt ◽  
Positional Control

Tissue identity determination is critical for regeneration, and the planarian anteroposterior (AP) axis uses positional control genes expressed from bodywall muscle to determine body regionalization. Canonical Wnt signaling establishes anterior versus posterior pole identities through notum and wnt1 signaling, and two Wnt/FGFRL signaling pathways control head and trunk domains, but their downstream signaling mechanisms are not fully understood. Here we identify a planarian Src homolog that restricts head and trunk identities to anterior positions. src-1(RNAi) animals formed enlarged brains and ectopic eyes and also duplicated trunk tissue, similar to a combination of Wnt/FGFRL RNAi phenotypes. src-1 was required for establishing territories of positional control gene expression, indicating it acts at an upstream step in patterning the AP axis. Double RNAi experiments and eye regeneration assays suggest src-1 can act in parallel to at least some Wnt and FGFRL factors. Co-inhibition of src-1 with other posterior-promoting factors led to dramatic patterning changes and a reprogramming of Wnt/FGFRLs into controlling new positional outputs. These results identify src-1 as a factor that promotes robustness of the AP positional system that instructs appropriate regeneration.

scholarly journals Discovery of gene regulatory elements through a new bioinformatics analysis of haploid genetic screens

2018 ◽  
Author(s):  
Bhaven B. Patel ◽  
Andres M. Lebensohn ◽  
Jan E. Carette ◽  
Julia Salzman ◽  
Rajat Rohatgi
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Insertional Mutagenesis ◽  
Bioinformatics Analysis ◽  
Regulatory Elements ◽  
Gene Trap ◽  
Genetic Screens ◽  
Control Gene ◽  
Protein Coding ◽  
Control Gene Expression

AbstractThe systematic identification of regulatory elements that control gene expression remains a challenge. Genetic screens that use untargeted mutagenesis have the potential to identify protein-coding genes, non-coding RNAs and regulatory elements, but their analysis has mainly focused on identifying the former two. To identify regulatory elements, we conducted a new bioinformatics analysis of insertional mutagenesis screens interrogating WNT signaling in haploid human cells. We searched for specific patterns of retroviral gene trap integrations (used as mutagens in haploid screens) in short genomic intervals overlapping with introns and regions upstream of genes. We uncovered atypical patterns of gene trap insertions that were not predicted to disrupt coding sequences, but caused changes in the expression of two key regulators of WNT signaling, suggesting the presence of cis-regulatory elements. Our methodology extends the scope of haploid genetic screens by enabling the identification of regulatory elements that control gene expression.

scholarly journals Epigenetics, Wnt signaling, and stem cells: the Pygo2 connection

2009 ◽  
Vol 185 (5) ◽  
pp. 761-763 ◽  
Author(s):  
Valerie Horsley
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Wnt Signaling ◽  
Chromatin Remodeling ◽  
Transcriptional Activation ◽  
Mammary Epithelial ◽  
Epigenetic Mechanisms ◽  
Control Gene ◽  
Epithelial Stem Cells ◽  
Control Gene Expression

Stem cells use both transcriptional and epigenetic mechanisms to control gene expression and regulate tissue development and homeostasis. In this issue, Gu et al. (Gu, B., P. Sun, Y. Yuan, R.C. Moraes, A. Li, A. Teng, A. Agrawal, C. Rhéaume, V. Bilanchone, J.M. Veltmaat, et al. 2009. J. Cell Biol. 185:811–826) reveal an important link between these two mechanisms in mammary epithelial stem cells by showing that transcriptional activation of β-catenin downstream of Wnt signaling can be regulated epigenetically through a chromatin remodeling factor, Pygo2.

LEC1 (NF-YB9) directly interacts with LEC2 to control gene expression in seed

2018 ◽  
Vol 1861 (5) ◽  
pp. 443-450 ◽  
Author(s):  
C. Boulard ◽  
J. Thévenin ◽  
O. Tranquet ◽  
V. Laporte ◽  
L. Lepiniec ◽  
...  
Keyword(s):  
Gene Expression ◽  
Control Gene ◽  
Control Gene Expression

scholarly journals Nonhistone Proteins Control Gene Expression in Reconstituted Chromatin

1974 ◽  
Vol 71 (12) ◽  
pp. 5057-5061 ◽  
Author(s):  
T. Barrett ◽  
D. Maryanka ◽  
P. H. Hamlyn ◽  
H. J. Gould
Keyword(s):  
Gene Expression ◽  
Control Gene ◽  
Nonhistone Proteins ◽  
Control Gene Expression

scholarly journals A Quantitative Optogenetic Tool to Control Gene Expression during Embryonic Development

2021 ◽  
Vol 120 (3) ◽  
pp. 354a
Author(s):  
Anand P. Singh ◽  
Ping Wu ◽  
Eric F. Wieschaus ◽  
Jared E. Toettcher ◽  
Thomas Gregor
Keyword(s):  
Gene Expression ◽  
Embryonic Development ◽  
Control Gene ◽  
Control Gene Expression

scholarly journals Chromatin-associated APC regulates gene expression in collaboration with canonical WNT signaling and AP-1

Oncotarget ◽  
2018 ◽  
Vol 9 (58) ◽  
pp. 31214-31230 ◽  
Author(s):  
William Hankey ◽  
Zhong Chen ◽  
Maxwell J. Bergman ◽  
Max O. Fernandez ◽  
Baris Hancioglu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Canonical Wnt Signaling ◽  
Canonical Wnt

scholarly journals Cellular FLIP Inhibits β-Catenin Ubiquitylation and Enhances Wnt Signaling

2004 ◽  
Vol 24 (19) ◽  
pp. 8418-8427 ◽  
Author(s):  
Mikihiko Naito ◽  
Ryohei Katayama ◽  
Toshiyasu Ishioka ◽  
Akiko Suga ◽  
Kohei Takubo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Responses ◽  
Wnt Signaling ◽  
Axis Formation ◽  
Caspase Activity ◽  
Additional Mechanism ◽  
Long Form ◽  
Fas Signaling ◽  
Canonical Wnt ◽  
Cellular Flip

ABSTRACT Cellular FLIP (cFLIP) is a close homologue of caspase 8 without caspase activity that inhibits Fas signaling. The cFLIP protein is often expressed in human tumors and is believed to suppress antitumor immune responses involving the Fas system. Here, we report that a long form of cFLIP (cFLIP-L) inhibits β-catenin ubiquitylation and increases endogenous cytosolic β-catenin, which results in translocation of β-catenin into nuclei and induction of β-catenin-dependent gene expression in cFLIP-L-expressing cells. When cells stably expressing cFLIP-L were stimulated with Wnt3a, enhanced Wnt signaling was observed compared with the control cells. Conversely, depletion of endogenous cFLIP results in reduced Wnt signaling. Furthermore, cFLIP-L increases secondary-body axis formation when coinjected with suboptimal doses of β-catenin into early Xenopus embryos. Down-regulation of FADD by RNA-mediated interference abolishes the β-catenin-dependent gene expression induced by cFLIP-L. These results indicate that cFLIP-L, in cooperation with FADD, enhances canonical Wnt signaling by inhibiting proteasomal degradation of β-catenin, thus suggesting an additional mechanism involved with tumorgenesis, in addition to inhibiting Fas signaling.

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