scholarly journals Downstream of a Kinase Cascade: A Trihelix Transcription Factor Represses Immune Genes

2015 ◽  
Vol 27 (3) ◽  
pp. 481-481
Author(s):  
Nancy R. Hofmann
2009 ◽  
Vol 21 (8) ◽  
pp. 2307-2322 ◽  
Author(s):  
Christian Breuer ◽  
Ayako Kawamura ◽  
Takanari Ichikawa ◽  
Rumi Tominaga-Wada ◽  
Takuji Wada ◽  
...  

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Zhiqiang Lin ◽  
Haidong Guo ◽  
Sylvia Zohrabian ◽  
Yuan Cao ◽  
William T. Pu

Binding of the transcription co-activator YAP with the transcription factor TEAD stimulates growth of the heart and other organs. Many signaling pathways, including the Hippo kinase cascade, converge to regulate YAP activity. However, less in known about the mechanisms that govern TEAD. YAP overexpression potently stimulates fetal cardiomyocyte (CM) proliferation, but YAP’s mitogenic potency declines postnatally, when mammalian cardiomyocytes largely exit the cell cycle. Here, we show that VGLL4, a CM-enriched TEAD1 binding protein, inhibits CM proliferation by limiting its binding to YAP and by targeting TEAD1 for degradation. VGLL4 antagonism of TEAD1 was governed by its acetylation at K225. Overexpression of VGLL4-K225R, an acetylation-refractory mutant, enhanced TEAD1 degradation, limited neonatal CM proliferation, and caused CM necrosis and heart failure. Our study defines an acetylation-mediated, VGLL4-dependent switch that regulates YAP-TEAD1 activity and restrains CM proliferation. These insights may enable more effective regulation of TEAD-YAP activity in applications ranging from cardiac regeneration to restraining cancer.


2020 ◽  
Vol 103 (4-5) ◽  
pp. 545-560
Author(s):  
Xiaoshuang Liu ◽  
Dechuan Wu ◽  
Tiaofeng Shan ◽  
Shanbin Xu ◽  
Ruiying Qin ◽  
...  

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Xiao-Hong Wang ◽  
Qing-Tian Li ◽  
Hao-Wei Chen ◽  
Wan-Ke Zhang ◽  
Biao Ma ◽  
...  

2021 ◽  
Vol 22 (22) ◽  
pp. 12137
Author(s):  
Peng Li ◽  
Zhaoxia Li ◽  
Guangning Xie ◽  
Juren Zhang

Maize kernels are the harvested portion of the plant and are related to the yield and quality of maize. The endosperm of maize is a large storage organ that constitutes 80–90% of the dry weight of mature kernels. Maize kernels have long been the study of cereal grain development to increase yield. In this study, a natural mutation that causes abnormal kernel development, and displays a shrunken kernel phenotype, was identified and named “shrunken 2008 (sh2008)”. The starch grains in sh2008 are loose and have a less proteinaceous matrix surrounding them. The total storage protein and the major storage protein zeins are ~70% of that in the wild-type control (WT); in particular, the 19 kDa and 22 kDa α-zeins. Map-based cloning revealed that sh2008 encodes a GT-2 trihelix transcription factor, ZmThx20. Using CRISPR/Cas9, two other alleles with mutated ZmThx20 were found to have the same abnormal kernel. Shrunken kernels can be rescued by overexpressing normal ZmThx20. Comparative transcriptome analysis of the kernels from sh2008 and WT showed that the GO terms of translation, ribosome, and nutrient reservoir activity were enriched in the down-regulated genes (sh2008/WT). In short, these changes can lead to defects in endosperm development and storage reserve filling in seeds.


2015 ◽  
Vol 66 (9) ◽  
pp. 2475-2485 ◽  
Author(s):  
Martin O’Brien ◽  
Ruth N. Kaplan-Levy ◽  
Tezz Quon ◽  
Pia G. Sappl ◽  
David R. Smyth

Sign in / Sign up

Export Citation Format

Share Document