
The graphic shows images of a cell under mtDNA replication stress made using so-called Correlative Light and Electron Microscopy (for short: CLEM). The mitochondrial DNA (mtDNA, green) is ejected from the mitochondria (magenta) and taken up by a lysosome, which contains the retromer (cyan). The highlighted section was also analysed using 3D-CLEM to obtain volumetric information.
Fig.: HHU/David Pla-Martín.
Yet Another Workaround for a Flawed Design.
Researchers led by Professor Dr David Pla-Martín of Heinrich Heine University Düsseldorf, alongside colleagues from the University of Cologne, have uncovered yet another complex but error-prone workaround—this time, to fix a problem that stems from an earlier design flaw.
They have identified a mechanism used to repair mitochondrial DNA (mtDNA) when it breaks. From an intelligent design perspective, mitochondria — once free-living bacteria—were supposedly the 'quick fix' to give eukaryotic cells the ability to efficiently convert glucose into adenosine triphosphate (ATP) using oxygen. ATP is the primary energy currency used in metabolic reactions, formed from adenosine diphosphate (ADP) and phosphate.
A truly intelligent designer, however, could have simply endowed cells with this biochemical machinery from the start—no need to incorporate foreign bacteria complete with their own DNA. But apparently, that would have been too simple.
This convoluted solution, predictably, comes with problems. Mitochondria often replicate their DNA imperfectly, or the DNA becomes damaged, leading to mitochondrial failure and a range of diseases. So, yet another layer of biological complexity has evolved to patch up the broken mtDNA. And, in classic Heath Robinson fashion, this repair mechanism is itself error-prone.