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Scientists uncover puzzling patterns in A-to-I mRNA editing that evolution alone can't fully explain.

A-to-I mRNA Editing

It is a process where cells modify the genetic instructions carried by messenger RNA (mRNA) before they are used to make proteins.

DNA contains genes— that instruct cells how to build proteins using 20 amino acids. These are written in a four-letter code: A (adenosine), T (thymine), G (guanine), and C (cytosine).

When a cell needs to make a protein, it copies a gene’s instructions from DNA into mRNA, which travels to the ribosome, the cell’s protein-making factory. 

• Sometimes, the cell changes an ‘A’ (adenosine) in the mRNA to ‘I’ (inosine) through a process called A-to-I mRNA editing. 
• This switch can alter the protein produced, as the code changes, resulting in a different amino acid being added to the protein.

This editing can have big effects. For example, certain mRNA codes, like UAG or UGA, signal the ribosome to stop building the protein. These are called stop codons. 

• If A-to-I editing changes UAG to UGG, the ribosome no longer stops but instead adds the amino acid tryptophan and continues building a longer protein.

Significance of A-to-I mRNA Editing

A-to-I mRNA editing adds flexibility to how cells use genetic information. It allows cells to produce different versions of proteins from the same gene, increasing diversity without changing the DNA itself.

In animals, proteins called ADARs (adenosine deaminases acting on RNA) carry out this editing, targeting double-stranded RNA, often in the brain, to support development and nervous system function. In fungi, different enzymes, like FgTad2-FgTad3, handle the editing, especially during sexual reproduction stages.

The process is evolutionarily conserved, meaning it has persisted across species for millions of years. But why does it exist when DNA could simply code for the desired protein directly? This question puzzles scientists, and recent research offers clues but no complete answers.

Recent Research from China

Researchers in China, have explored A-to-I mRNA editing in animals and fungi, particularly in the fungus Fusarium graminearum, which infects wheat and barley crops.

Fungal Editing Mechanism:

Unlike animals, fungi lack ADAR enzymes. Instead, a protein complex called FgTad2-FgTad3, along with a sexual stage-specific protein Ame1, drives A-to-I mRNA editing in Fusarium graminearum.  

The editing is regulated through alternative promoters, translation initiation, and post-translational modifications, ensuring it happens only at specific times.  

Adaptive Advantage

Studies show that A-to-I editing in fungi is non-synonymous, meaning it changes the amino acid sequence of proteins.

Mutants with only edited or unedited versions of these genes struggle to reproduce, while those with both versions grow, confirming that editing provides a flexible advantage over fixed DNA mutations.

In Fusarium graminearum, editing helps the fungus balance survival and reproduction. For example, unedited versions of genes PSC69 and PSC64 help the fungus resist environmental stresses during its vegetative (growth) stage, while edited versions support sexual development.

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Source: 

THE HINDU