Washington, September 4 (ANI): In a new research, scientists have discovered that a duplicate copy of a gene involved in embryonic development of fish has taken up a newer role in the evolution of fish scales.

Scientists have suspected that spare parts in the genome-extra copies of functional genes that arise when genes or whole genomes get duplicated-might sometimes provide the raw materials for the evolution of new traits.

Now, researchers say that they have discovered a prime example of this in fish.

The researchers show that a duplicate copy of a gene involved in embryonic development has taken up a newer and decidedly less essential role in the development of fish scales.

Zebrafish carrying a mutant version of that extra fibroblast growth factor receptor 1 (fgfr1) gene show decreases in their scale formation.

What’s more, the spare fgfr1 gene is at the root of similar scale loss seen in domesticated carp, which have been selectively bred by humans for the last 2,000 years.

“Our finding is an excellent case for (gene) duplication supporting diverse forms,” said Matthew Harris of the Max Planck Institute for Developmental Biology.

“By ‘tweaking’ the use of one of the two copies of the fish fgfr1, the teleost order that contains zebrafish and carp have a specialized ‘toolbox’ gene that now controls adult-specific variation in form,” added Nicolas Rohner, also of the Max Planck Institute.

Fish species outnumber all other vertebrates combined and include many with spectacular features to match the diverse environments in which they live, according to Harris and Rohner.

Teleost fish in particular represent the largest assemblage of vertebrates, comprising over 26,000 species with astonishing diversity in their form and physiology.

Although little is known about the genetic basis of that diversity, it is clear that gene duplication is commonplace within teleost groups, providing a source of genetic raw material for selection.

To further explore in the new study, the researchers first examined mutant strains of zebrafish in search of those with changes to their fins, skulls, or scales, all structures that tend to vary among species.

They focused their attention on one with fewer scales and in an unusual pattern-an abnormality they traced to fgfr1.

“We were surprised to find severe coding mutations in such an important developmental gene to cause an adult-specific and viable phenotype,” Harris said.

Further study showed the reason why: zebrafish maintain two copies of fgfr1 that function redundantly during embryonic development. One of those two genes is also required for the formation of the scales in juveniles. (ANI)