scholarly journals Drosophila SETDB 1 and caspase cooperatively fine‐tune cell fate determination of sensory organ precursor

2016 ◽  
Vol 21 (4) ◽  
pp. 378-386 ◽  
Author(s):  
Natsuki Shinoda ◽  
Fumiaki Obata ◽  
Liu Zhang ◽  
Masayuki Miura
2014 ◽  
Vol 19 (3) ◽  
pp. 239-253 ◽  
Author(s):  
Shohei Murakami ◽  
Ritsuko Shimizu ◽  
Paul-Henri Romeo ◽  
Masayuki Yamamoto ◽  
Hozumi Motohashi

2016 ◽  
Vol 104 (3) ◽  
pp. 324-329 ◽  
Author(s):  
Shin’ichiro Yasunaga ◽  
Yoshinori Ohno ◽  
Naoto Shirasu ◽  
Bo Zhang ◽  
Kyoko Suzuki-Takedachi ◽  
...  

10.1038/ni793 ◽  
2002 ◽  
Vol 3 (5) ◽  
pp. 443-450 ◽  
Author(s):  
Kenji Tanigaki ◽  
Hua Han ◽  
Norio Yamamoto ◽  
Kei Tashiro ◽  
Masaya Ikegawa ◽  
...  

2019 ◽  
Vol 10 (9) ◽  
Author(s):  
Lan-Hsin Wang ◽  
Nicholas E. Baker

Abstract The fundamental roles for the Salvador–Warts–Hippo (SWH) pathway are widely characterized in growth regulation and organ size control. However, the function of SWH pathway is less known in cell fate determination. Here we uncover a novel role of the SWH signaling pathway in determination of cell fate during neural precursor (sensory organ precursor, SOP) development. Inactivation of the SWH pathway in SOP of the wing imaginal discs affects caspase-dependent bristle patterning in an apoptosis-independent process. Such nonapoptotic functions of caspases have been implicated in inflammation, proliferation, cellular remodeling, and cell fate determination. Our data indicate an effect on the Wingless (Wg)/Wnt pathway. Previously, caspases were proposed to cleave and activate a negative regulator of Wg/Wnt signaling, Shaggy (Sgg)/GSK3β. Surprisingly, we found that a noncleavable form of Sgg encoded from the endogenous locus after CRISPR-Cas9 modification supported almost normal bristle patterning, indicating that Sgg might not be the main target of the caspase-dependent nonapoptotic process. Collectively, our results outline a new function of SWH signaling that crosstalks to caspase-dependent nonapoptotic signaling and Wg/Wnt signaling in neural precursor development, which might be implicated in neuronal pathogenesis.


RSC Advances ◽  
2019 ◽  
Vol 9 (64) ◽  
pp. 37300-37311 ◽  
Author(s):  
Zixiang Wu ◽  
Shujing Liang ◽  
Wenyu Kuai ◽  
Lifang Hu ◽  
Airong Qian

The recent advances of miRNAs and lncRNAs in determining the cell fate of MSCs.


2005 ◽  
Vol 25 (21) ◽  
pp. 9460-9468 ◽  
Author(s):  
Anita Borton Hjelmeland ◽  
Stephen H. Schilling ◽  
Xing Guo ◽  
Darryl Quarles ◽  
Xiao-Fan Wang

ABSTRACT Runx2 is required for osteoblast differentiation but is expressed in certain nonosteoblastic cells without activating the differentiation process, suggesting that its activity is suppressed through a lineage-specific mechanism. Here we report that primary mouse dermal fibroblasts lacking Smad3 can acquire an osteoblast-like phenotype, including activation of Runx2 activity, expression of osteoblast-specific genes, and calcium deposition. We further show that negative regulation of Runx2 activity by Smad3 in dermal fibroblasts is likely mediated by controlling the expression of Msx2, an antagonist of Runx2 in this cellular context. These data support the presence of a novel mechanism for controlling cell fate determination of mesenchymal lineages by preventing differentiation toward the osteoblastic lineage via negative regulation of Runx2 activity.


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