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NTR: protein-mitochondrial outer membrane tethering activity #29131
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I have cpc2 (RAC K1) annotated as "ribosome binding" but RACK1 is sometimes described as a "ribosome receptor" due to its dual role: it serves both as a core ribosomal component and as a scaffold for recruiting other signaling proteins to the ribosome. The term "receptor" in this context emphasizes RACK1's function in docking signaling molecules (like kinases) onto the ribosome, enabling signal transduction pathways to directly influence translation. So, I guess the ribosome binding annotations. should be removed. Also, consider a general parent of mitochondrion outer membrane-hibernating ribosome tether activity ribosome adaptor exact synonym ribosome receptor |
I guess for this I can use |
If we made the term: |
Good point, we dont have an activity that describes a single gene product. |
Please provide as much information as you can:
NTR: mitochondrion-hibernating ribosome tether activityNTR protein-mitochondrial outer membrane tethering activity
The binding activity of a molecule that brings together a protein or protein complex and a mitochondrial outer membrane lipid or membrane-associated protein, in order to maintain the localization of the protein, or protein complex at a specific mitochondrial outer membrane location.
definition adapted from
cytoskeleton protein-membrane anchor activity
PMID:39379376
Title | Ribosomes hibernate on mitochondria during cellular stress.
https://europepmc.org/article/MED/39379376#free-full-text
pretty electron tomography
https://www.pombase.org/gene/SPAC6B12.15
GO:0043495 | protein-membrane adaptor activity
Children terms (if applicable) Should any existing terms that should be moved underneath this new proposed term?
Any other information
We then used in situ cryo-ET to assess whether ribo- somal tethering to mitochondria was affected in the Δcpc2 strain. The tomograms showed fragmented circular mitochondria, as observed in WT cells, while no ribosome tethering was observed after 7 days of cells growing at low glucose concentrations (Fig. 5c, d, Supplementary Fig. 10 and Supplementary Movie 3).
Therefore, our data reveals a distinct mode of interaction between ribosomes and mitochondria, which is disrupted by the deletion of Cpc2. Our results indicate that Cpc2 is implicated in both cell viability and ribosome tethering to mitochondria under glucose depletion conditions, emphasizing its key role in mitochondrial homeostasis.
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