The New Zealand Herald

Kiwi boffins in DNA discovery

Researcher­s’ finding could open door to breakthrou­gh on understand­ing disease

- Jamie Morton

What we know about diseases as common as cancer, diabetes and dementia could be transforme­d following ground-breaking findings by Kiwi researcher­s.

The new study by scientists from Auckland University’s Liggins Institute, Otago University and Massey University has revealed fresh insights into mitochondr­ia and the littleunde­rstood role they play in the developmen­t of our bodies.

Measuring just a 1000th of a millimetre each, mitochondr­ia DNA are specialise­d sub-units of cells that act as their batteries or generators, as they supply most of the cell’s energy.

The more energy-hungry a type of cell is, the more mitochondr­ia it contains, ranging from several to thousands of them.

We receive the DNA in our cells’ nuclei — organised into chromosome­s — from both parents, but we inherit our mitochondr­ial DNA from our mothers only.

Mutations in the mitochondr­ial DNA are relatively common, affecting one in a few thousand people, and are linked to common illnesses along with a wide range of fatal or progressiv­ely debilitati­ng diseases, including diabetes, gastrointe­stinal disorders, heart disease, dementia, deafness, and eye disorders.

But now there are new reasons to suspect their roles in disorders.

In their new study, published in the journal Mitochondr­ion, the researcher­s have shown for the first time that human mitochondr­ial DNA leaves the mitochondr­ia, travels into the host cell nucleus and connects to specific genes.

“We found evidence that mitochondr­ia DNA and nuclear DNA ‘talk Researcher­s have shown for the first time in humans that mitochondr­ial DNA travels into the host cell nucleus and “talks to” specific genes on the DNA. Mitochondr­ial DNA may influence gene expression. This finding could be a key to understand­ing how mitochondr­ial DNA mutations manifest as disease. to each other’, and these interactio­ns aren’t random,” said lead researcher Dr Justin O’Sullivan, a Liggins molecular geneticist.

The findings give weight to the idea that mitochondr­ia do much more than supply energy and regulate a cell’s metabolism — the processes that keep it alive.

“We think the connection­s we detected are part of a feedback system between mitochondr­ia and the cell nucleus that may influence how humans grow and develop throughout life,” O’Sullivan said.

Interactio­ns between the two sets of DNA within our cells could be one of the ways the environmen­t influences gene expression, he said.

One theory about mitochondr­ial disease is that the damaged -mitochondr­ia fail to supply enough energy to the cell so it can’t work properly.

But this latest finding suggests another possible culprit: problems with the way the mitochondr­ial and nuclei DNA “talk” to each other — or fail to talk to each other.

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