scholarly journals A role for post-transcriptional control of endoplasmic reticulum dynamics and function inC. elegansgermline stem cell maintenance

Development ◽  
2016 ◽  
Vol 143 (17) ◽  
pp. 3097-3108 ◽  
Author(s):  
Richa Maheshwari ◽  
Kumari Pushpa ◽  
Kuppuswamy Subramaniam
2022 ◽  
Author(s):  
Ishara S Ariyapala ◽  
Kasun Buddika ◽  
Heather A Hundley ◽  
Brian Calvi ◽  
Nicholas Sokol

The regulation of stem cell survival, self-renewal, and differentiation is critical for the maintenance of tissue homeostasis. Although the involvement of signaling pathways and transcriptional control mechanisms in stem cell regulation have been extensively investigated, the role of post-transcriptional control is still poorly understood. Here we show that the nuclear activity of the RNA-binding protein Second Mitotic Wave Missing (Swm) is critical for Drosophila intestinal stem cells (ISCs) and their daughter cells, enteroblasts (EBs), to maintain their identity and function. Loss of swm in these intestinal progenitor cells leads ISCs and EBs to lose defined cell identities, fail to proliferate, and detach from the basement membrane, resulting in severe progenitor cell loss. swm loss further causes nuclear accumulation of poly(A)+ RNA in progenitor cells. Swm associates with transcripts involved in epithelial cell maintenance and adhesion, and the loss of swm, while not generally affecting the levels of these Swm-bound mRNAs, leads to elevated expression of proteins encoded by some of them, including the fly orthologs of Filamin and Talin. Taken together, this study indicates a role for Swm in adult stem cell maintenance, and raises the possibility that nuclear post-transcriptional gene regulation plays vital roles in controlling adult stem cell maintenance and function.


Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2812-2822 ◽  
Author(s):  
Tao Wang ◽  
Vijayalakshmi Nandakumar ◽  
Xiao-Xia Jiang ◽  
Lindsey Jones ◽  
An-Gang Yang ◽  
...  

Key Points Mysm1 is required to maintain the quiescence and pool size of HSC, and its deletion severely impairs the survival and function of HSC. Mysm1 controls HSC homeostasis by regulating Gfi1 expression via modulating histone modifications and transcriptional factors recruitment.


Bone ◽  
2013 ◽  
Vol 54 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Brahmananda R. Chitteti ◽  
Ying-Hua Cheng ◽  
Melissa A. Kacena ◽  
Edward F. Srour

2010 ◽  
Vol 123 (5) ◽  
pp. e1-e1
Author(s):  
A. J. Bardin ◽  
C. N. Perdigoto ◽  
T. D. Southall ◽  
A. H. Brand ◽  
F. Schweisguth

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Na Liu ◽  
Rui Yang ◽  
Ying Shi ◽  
Ling Chen ◽  
Yating Liu ◽  
...  

Abstract Posttranslational modifications (PTMs) of proteins, including chromatin modifiers, play crucial roles in the dynamic alteration of various protein properties and functions including stem-cell properties. However, the roles of Lymphoid-specific helicase (LSH), a DNA methylation modifier, in modulating stem-like properties in cancer are still not clearly clarified. Therefore, exploring PTMs modulation of LSH activity will be of great significance to further understand the function and activity of LSH. Here, we demonstrate that LSH is capable to undergo PTMs, including methylation and phosphorylation. The arginine methyltransferase PRMT5 can methylate LSH at R309 residue, meanwhile, LSH could as well be phosphorylated by MAPK1 kinase at S503 residue. We further show that the accumulation of phosphorylation of LSH at S503 site exhibits downregulation of LSH methylation at R309 residue, which eventually promoting stem-like properties in lung cancer. Whereas, phosphorylation-deficient LSH S503A mutant promotes the accumulation of LSH methylation at R309 residue and attenuates stem-like properties, indicating the critical roles of LSH PTMs in modulating stem-like properties. Thus, our study highlights the importance of the crosstalk between LSH PTMs in determining its activity and function in lung cancer stem-cell maintenance.


Development ◽  
2010 ◽  
Vol 137 (5) ◽  
pp. 705-714 ◽  
Author(s):  
A. J. Bardin ◽  
C. N. Perdigoto ◽  
T. D. Southall ◽  
A. H. Brand ◽  
F. Schweisguth

Blood ◽  
2013 ◽  
Vol 121 (6) ◽  
pp. 918-929 ◽  
Author(s):  
Sung-Uk Lee ◽  
Manami Maeda ◽  
Yuichi Ishikawa ◽  
Sierra Min Li ◽  
Anne Wilson ◽  
...  

Key Points Notch1/DII4-mediated signals are normally suppressed by LRF, preventing HSCs from premature T-cell differentiation in the bone marrow. Erythroblastic islands may have the capacity to regulate the fate and function of HSCs.


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