New clues to how plants retain healthy genomes, avoid mitochondrial disease
MSH1 repairs organelle DNA. The MSH1 protein slides along a DNA strand until it detects mutations. Then MSH1 cuts both strands of DNA. The DNA repair machinery in the cell uses homologous DNA (DNA of the same sequence) as a template to fix the mutation. B) MSH1 increases sorting of organelle DNA. A population of green (normal) and blue (mutant) organelle DNA molecules is shown. When functional MSH1 is present, it homogenizes copies of DNA, and the resulting populations contain either normal or mutant DNA. When MSH1 is absent, the DNA types remain mixed. Credit: Colorado State University

About 1 in every 4,300 people in the United States are affected by the destruction of the mitochondria.

Poor growth, muscle weakness, neurological problems and more can be caused by diseases in which the genes inside the cell's mitochondria are found. Nuclear genomes are related to the mother and father, butMitochondrial genomes are related to the mother and father.

Mitochondrial genomes in humans and other animals are very high and can be easily passed on to children. Scientists want to learn more about why these high rates occur and what can be done to stop them so that they don't happen again.

Colorado State University biologists are looking for answers to questions that are not related to medicine. Humans have a lot to learn from plants when it comes to keeping their genomes free of disease-causing genes.

How do plants change their genetic makeup?

A recent study led by a research scientist in the lab of an associate professor in the Department of Biology sheds new light on how plants usually don't experience genetic changes. Plants are able to fix these problems quickly and not pass on the problem to their offspring.

In the past, Sloan and his lab members have hypothesised that genes responsible for repair and recombination in plant cells might be involved in keeping these cells healthy and free of disease. The MSH1 is a genes found in plants but not humans. They found that this gene is critical for keeping the rate ofMitochondrial Variation low in plants.

They wanted to understand how the genes of the plant and its descendants spread. According to their new paper, plants are very good at sorting normal and disease-causing genes. Natural selection takes over after the sorting process because offspring that inherit disease-causing genes are less likely to live.

The ability to sort is less effective than the ability to mix up the good and bad in humans. Plants remove heteroplasmy from their cells much more quickly than animals and humans.

The researchers used a sensitive technique called digital droplet PCR to track the genetic changes they found in the plant. They were able to analyze the amount of normal and mutant genes in these plants.

The biologists at Colorado State University found that functional copies of MSH1 speed up the process of DNA sorting in plants. MSH1 is thought to be responsible for first identifying and fixing genetic defects. MSH1 can be used to sort out amutations if they persist for one reason or another.

It shows how nature has devised multiple ways of dealing with organelle genomes. One of the factors leading to aging and disease in humans is the fact that there are a lot of Mitochondrial Tumours. Knowing how plants and other organisms maintain low mitochondria rates can help us understand how this process goes awry in humans and how it can be fixed.

They have more to learn from their plants. They are creating a mathematical model that will try to understand what cellular forces are responsible for the different rates of organelle DNA sorting in plants. The University of Bergen is leading that part of the project. They want to find out if MSH1 has the same effect on sorting mitochondrial DNA in other plant types, like trees that have different development patterns.

More information: Amanda K. Broz et al, Sorting of mitochondrial and plastid heteroplasmy in Arabidopsis is extremely rapid and depends on MSH1 activity, Proceedings of the National Academy of Sciences (2022). DOI: 10.1073/pnas.2206973119 Journal information: Proceedings of the National Academy of Sciences