The genes of the mitochondrion (kinetoplast) of some Kinetoplastida - e.g. Trypa

Question

The genes of the mitochondrion (kinetoplast) of some Kinetoplastida - e.g. Trypanosoma brucei, the parasite which causes African sleeping sickness - are "encoded" in a way that the pre mRNA requiries partially heavy editing (insertion and deletion of Uridines) by the editosome (a RNA/Protein complex) until it can be translated to the correct proteins. The information where to insert and remove Uridines is contained in small gRNA also part of the mitochondrial genome.

However this whole thing seems kind of unnecessary to me. Why did evolution not get rid of the surplus/missing Thymidines in those Genes? What's the use of this?

Explanation / Answer

You could have asked a similar question about splicing. The function of RNA editing seems to be similar: it's one of the ways to trigger production of alternative transcripts and proteins given the same DNA sequence.

The question is discussed, for example, in this review. The authors describe different known effects of alternative RNA editing:

Amino-acid substitutions
ORF extension
New unique ORFs
Alternative UTRs

Alternative editing is correlated with developmental stage, which is not surprising, given the fact that the parasites switch their energy metabolism in different hosts (1,2,3), with the mitochondria changing their structure accordingly.

The authors seem to be astonished as well and conclude: "RNA editing in kinetoplastid mitochondria is a beautiful example how evolution favors diversifying mechanisms even if they seem to be extremely wasteful from a human perspective."

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