Rewired for Romance: Scientists Give Gift-Giving Behavior to Singing Fruit Flies

In a groundbreaking study published in the journal Science, researchers from Japan have successfully transferred a unique courtship behavior from one species of fruit fly to another. By activating a single gene in insulin-producing neurons, the team made Drosophila melanogaster, a species that typically sings “courtship songs,” perform a gift-giving ritual it had never done before.

The study reveals that the reason for this difference lies in the connection between insulin-producing neurons and the courtship control center in the brain. In gift-giving flies (D. subobscura), these cells are connected, while in singing flies (D. melanogaster), they remain disconnected. This discovery highlights that the evolution of novel behaviors does not necessarily require the emergence of new neurons; instead, small-scale genetic rewiring can lead to behavioral diversification and species differentiation.

The researchers inserted DNA into D. subobscura embryos to create flies with heat-activated proteins in specific brain cells. They used heat to activate groups of these cells and compared the brains of flies that did and did not regurgitate food. The study identified 16-18 insulin-producing neurons that make the male-specific protein FruM, clustered in a part of the brain called the pars intercerebralis.

“Our findings indicate that the evolution of novel behaviors does not necessarily require the emergence of new neurons; instead, small-scale genetic rewiring in a few preexisting neurons can lead to behavioral diversification and, ultimately, contribute to species differentiation,” said Dr. Yusuke Hara, co-lead author from the National Institute of Information and Communications Technology (NICT).

This study demonstrates how scientists can trace complex behaviors like nuptial gift-giving back to their genetic roots to understand how evolution creates entirely new strategies that help species survive and reproduce.

The research was conducted with support from KAKENHI Grant-in-Aid for Scientific Research and has been published in the journal Science on August 14, 2025.

The accelerated evolution engine known as T7-ORACLE has revolutionized the field of medicine and biotechnology by allowing researchers to evolve proteins with new or improved functions at an unprecedented rate. This breakthrough was achieved by Scripps Research scientists who have developed a synthetic biology platform that enables continuous evolution inside cells without damaging the cell’s genome.

Directed evolution is a laboratory process where mutations are introduced, and variants with improved function are selected over multiple cycles. Traditional methods require labor-intensive steps and can take weeks or more to complete. In contrast, T7-ORACLE accelerates this process by enabling simultaneous mutation and selection with each round of cell division, making it possible to evolve proteins continuously and precisely inside cells.

T7-ORACLE circumvents the bottlenecks associated with traditional approaches by engineering E. coli bacteria to host a second, artificial DNA replication system derived from bacteriophage T7. This allows for continuous hypermutation and accelerated evolution of biomacromolecules, making it possible to evolve proteins in days instead of months.

To demonstrate the power of T7-ORACLE, researchers inserted a common antibiotic resistance gene into the system and exposed E. coli cells to escalating doses of various antibiotics. In less than a week, the system evolved versions of the enzyme that could resist antibiotic levels up to 5,000 times higher than the original.

The broader potential of T7-ORACLE lies in its adaptability as a platform for protein engineering. Scientists can insert genes from humans, viruses, or other sources into plasmids and introduce them into E. coli cells, which are then mutated by T7-ORACLE to generate variant proteins that can be screened or selected for improved function.

This could help scientists more rapidly evolve antibodies to target specific cancers, evolve more effective therapeutic enzymes, and design proteases that target proteins involved in cancer and neurodegenerative disease. The system’s ease of implementation, combined with its scalability, makes it a valuable tool for advancing synthetic biology.

The research team is currently focused on evolving human-derived enzymes for therapeutic use and tailoring proteases to recognize specific cancer-related protein sequences. In the future, they aim to explore the possibility of evolving polymerases that can replicate entirely unnatural nucleic acids, opening up possibilities in synthetic genomics.

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Nature’s Armor: Scientists Uncover Gene Behind Aussie Skinks’ Immunity to Deadly Snake Venom

In a groundbreaking study led by the University of Queensland, scientists have discovered the genetic secret behind Australian skinks’ remarkable ability to withstand deadly snake venom. The research, published in the International Journal of Molecular Sciences, reveals that these small lizards have evolved a molecular armor to protect themselves from the toxic effects of neurotoxins.

Professor Bryan Fry from UQ’s School of the Environment explained that the skinks’ defense mechanism involves tiny changes in a critical muscle receptor called the nicotinic acetylcholine receptor. This receptor is normally targeted by snake venom, which blocks nerve-muscle communication and leads to rapid paralysis and death. However, in a stunning example of evolutionary adaptation, researchers found that skinks independently developed mutations on 25 occasions to block venom from attaching.

“It’s a testament to the massive evolutionary pressure exerted by venomous snakes after their arrival and spread across the Australian continent,” Professor Fry said. “The same mutations evolved in other animals like mongooses, which feed on cobras.”

Researchers confirmed that Australia’s Major Skink (Bellatorias frerei) has developed exactly the same resistance mutation as the honey badger, famous for its immunity to cobra venom.

To validate these findings, scientists conducted functional testing at UQ’s Adaptive Biotoxicology Laboratory. Dr. Uthpala Chandrasekara led the laboratory work and reported that the data was “crystal clear.” The modified receptors simply didn’t respond to toxins, demonstrating their remarkable ability to repel deadly snake venom.

This research has significant implications for biomedical innovation, particularly in the development of novel antivenoms or therapeutic agents. Dr. Chandrasekara emphasized that understanding how nature neutralizes venom can provide valuable clues for designing more effective treatments.

The project involved collaborations with museums across Australia and offers a promising example of interdisciplinary research, bridging the gap between scientific discovery and potential applications.