Faculty Opinions recommendation of TTC5 mediates autoregulation of tubulin via mRNA degradation.

Author(s):  
Sutapa Chakrabarti
Keyword(s):  
2021 ◽  
pp. 107805
Author(s):  
Charlotte Roux ◽  
Thibault Etienne ◽  
Eliane Hajnsdorf ◽  
Delphine Ropers ◽  
A.J. Carpousis ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shiho Makino ◽  
Tomoko Kawamata ◽  
Shintaro Iwasaki ◽  
Yoshinori Ohsumi

AbstractSynthesis and degradation of cellular constituents must be balanced to maintain cellular homeostasis, especially during adaptation to environmental stress. The role of autophagy in the degradation of proteins and organelles is well-characterized. However, autophagy-mediated RNA degradation in response to stress and the potential preference of specific RNAs to undergo autophagy-mediated degradation have not been examined. In this study, we demonstrate selective mRNA degradation by rapamycin-induced autophagy in yeast. Profiling of mRNAs from the vacuole reveals that subsets of mRNAs, such as those encoding amino acid biosynthesis and ribosomal proteins, are preferentially delivered to the vacuole by autophagy for degradation. We also reveal that autophagy-mediated mRNA degradation is tightly coupled with translation by ribosomes. Genome-wide ribosome profiling suggested a high correspondence between ribosome association and targeting to the vacuole. We propose that autophagy-mediated mRNA degradation is a unique and previously-unappreciated function of autophagy that affords post-transcriptional gene regulation.


Author(s):  
Nicky Hwang ◽  
Liren Sun ◽  
Daisy Noe ◽  
Patrick Y. S. Lam ◽  
Tianlun Zhou ◽  
...  
Keyword(s):  

Nature ◽  
2019 ◽  
Vol 568 (7751) ◽  
pp. 193-197 ◽  
Author(s):  
Mohamed A. El-Brolosy ◽  
Zacharias Kontarakis ◽  
Andrea Rossi ◽  
Carsten Kuenne ◽  
Stefan Günther ◽  
...  

2005 ◽  
Vol 25 (8) ◽  
pp. 3232-3246 ◽  
Author(s):  
Tae-Don Kim ◽  
Jong-So Kim ◽  
Jong Heon Kim ◽  
Jihwan Myung ◽  
Hee-Don Chae ◽  
...  

ABSTRACT Serotonin N-acetyltransferase (arylalkylamine N-acetyltransferase [AANAT]) is the key enzyme in melatonin synthesis regulated by circadian rhythm. To date, our understanding of the oscillatory mechanism of melatonin has been limited to autoregulatory transcriptional and posttranslational regulations of AANAT mRNA. In this study, we identify three proteins from pineal glands that associate with cis-acting elements within species-specific AANAT 3′ untranslated regions to mediate mRNA degradation. These proteins include heterogeneous nuclear ribonucleoprotein R (hnRNP R), hnRNP Q, and hnRNP L. Their RNA-destabilizing function was determined by RNA interference and overexpression approaches. Expression patterns of these factors in pineal glands display robust circadian rhythm. The enhanced levels detected after midnight correlate with an abrupt decline in AANAT mRNA level. A mathematical model for the AANAT mRNA profile and its experimental evidence with rat pinealocytes indicates that rhythmic AANAT mRNA degradation mediated by hnRNP R, hnRNP Q, and hnRNP L is a key process in the regulation of its circadian oscillation.


1992 ◽  
Vol 226 (3) ◽  
pp. 581-596 ◽  
Author(s):  
Oleg Yarchuk ◽  
Nathalie Jacques ◽  
Jean Guillerez ◽  
Marc Dreyfus
Keyword(s):  

1992 ◽  
Vol 3 (5) ◽  
pp. 535-544 ◽  
Author(s):  
B C Gliniak ◽  
L S Park ◽  
L R Rohrschneider

The murine myeloid precursor cell line FDC-P1/MAC simultaneously expresses receptors for multi-colony-stimulating factor (CSF), granulocyte-macrophage (GM)-CSF, and macrophage (M)-CSF. Growth of FDC-P1/MAC cells in either multi-CSF or GM-CSF results in the posttranscriptional suppression of M-CSF receptor (c-fms proto-oncogene) expression. We use the term transregulation to describe this control of receptor expression and have further characterized this regulatory process. The removal of FDC-P1/MAC cells from GM-CSF stimulation resulted in the re-expression of c-fms mRNA independent of M-CSF stimulation and new protein synthesis. Switching FDC-P1/MAC cells from growth in M-CSF to GM-CSF caused the selective degradation of c-fms mRNA within 6 h after factor switching. Blocking protein synthesis or gene transcription with metabolic inhibitors effectively prevented GM-CSF stimulated degradation of c-fms mRNA. These results suggest that the transregulation of c-fms transcripts by GM-CSF requires the transcriptional activation of a selective mRNA degradation factor. In vitro analysis, the use of cytoplasmic cell extracts, provided evidence that a ribonuclease is preferentially active in GM-CSF stimulated cells, although the specificity for mRNA degradation in vitro is broader than seen in vivo. Together, these data suggest that GM-CSF can dominantly transregulate the level of c-fms transcript through the transcriptional activation of a ribonuclease degradation system.


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