You must wonder if human will evolve again after we evolve from apes. In most of nature, natural selection and “survival of the fittest” still play a big role. Only the strongest can live in the wild. A few hundred years ago, humans were the same way, but what about now?
Now that we have better health care, food, heating, and hygiene, the number of “hazards” in our lives has dropped by a huge amount. These dangers are called “selection pressures” in the scientific world. They make it hard for us to stay alive in our environment and have children. “Survival of the fittest” is driven by selection pressure. This is how we became the species we are today.
Now that there are fewer forces of natural selection and more medicine and science to help us, the question is whether evolution will ever stop for humans. Is it already over? Will humans evolve again?
Will Human Evolve Again?
Genetic research has shown that humans are still changing. And we found some more new evidence in microgenes, which researchers are unfamiliar with.
humans are still developing new genes.
According to a new study, “De novo birth of functional microproteins in the human lineage” published in Cell Reports on Dec. 20, humans are still developing new genes. According to the researchers, at least 155 human genes arose from previously thought-of “junk” DNA sections as our ancestors progressed, including two human-specific genes that appeared after humans split from chimps around 4-6 million years ago.
“I felt it was a fantastic study,” says Alan Saghatelian, a Salk Institute biologist who was not engaged in the research. He goes on to say that he “wouldn’t be astonished” if a lot more of these genes were lying in plain sight.
sORFs have long been thought to be nonfunctional
The genes revealed in the current study stayed unknown for so long because they are so short: they are just around 300 nucleotides long, whereas the usual human gene is 10 to 15,000 base pairs long. Even though they feature start and stop codons that allow them to be read by cells’ transcriptional machinery exactly like regular genes, Saghatelian says that these so-called microgenes—also known as short open reading frames (sORFs)—have long been thought to be nonfunctional.
sORF – Short Open Reading Frame
A short open reading frame (sORF) is 300 bases long and encodes a microprotein or sORF-encoded protein (SEP) of 100 amino acids. Genome annotation pipelines have always written off sORFs as meaningless noise. However, ribosome profiling (RIBO-Seq), which found sORF-based transcripts in different parts of the genome, showed that sORFs could be used to coding.
Conventionally, an ORF is a string of nucleotide triplets (codons) that can be turned into proteins. It should start with an in-frame start codon (AUG) and end with one of the three stop codons (UAA, UAG, or UGA).
Theoretically, there is a 1 in 64 chance that a start codon will randomly appear in the nucleotide space, and there is a 99% chance that a stop codon will appear in the next 99 codons, ignoring splice variants, reading frames, GC-rich regions, strandedness, and nucleotide biases.
This means that only about 1.5% of the genome can code for ORFs with fewer than 100 codons. Because of this, there are an unreasonably large number of putative sORFs, and it seems unlikely that they will be transcribed and translated into functional polypeptides. So, a cutoff of 300 nucleotides was put in place because most of these sORFs were thought to be meaningless and random.
SORFs play an important role in human evolution
Recent research titled “Noncanonical open reading frames encode functional proteins essential for cancer cell survival” has found that turning off SORFs stops cell growth, which shows that they are, in fact, important. For example, a 2020 study found hundreds of working sORFs in human cells, both in areas of the genome that code for proteins and in areas that don’t. The number was surprising to Nikolaos Vakirlis, a computational evolutionary biologist at the Biomedical Sciences Research Center Alexander Fleming in Vari, Greece. He and his coworkers felt compelled to find out more about these strange genetic differences, which led to the research that was just published. “Species-specific genes are found everywhere,” Vakirlis explains. “There must have been an evolutionary path for them to take.”
Using data from the 2020 project, the scientists looked at the genomes of both humans and animals to find sORFs that worked and made proteins. Then, they used what they already knew about how humans and animals evolved to figure out the links between the sORFs based on when new microgenes appeared in evolution.
The scientists discovered 155 microgenes shared by all vertebrates via this method. According to prior research, 44 of these are essential for cell development. Three of them had signs of diseases like muscular dystrophy, retinitis pigmentosa, and Alazami syndrome. The researchers also found a microgene linked to human heart tissue that appeared when chimps and humans split from gorillas about 7 to 9 million years ago.
Vakirlis and his colleagues were surprised to find that these new genes did not come from mutations or duplications of existing genes, but rather from non-coding parts of DNA. Gene duplication is thought to be the main way that new genes are made in all species. However, the appearance of microgenes may explain how humans and other animals got traits that are only found in their species.
“This study is really important work,” says John Prensner, a physician at the Dana-Farber Cancer Institute and postdoctoral research fellow at the Broad Institute. He explains that scientists have known about sORFs and other non-canonical open reading frames for some time but haven’t determined what they might do. He demonstrates that microgenes are still a possible avenue for evolution today. They encode “proto-proteins,” or tiny proteins that organisms are only starting to experiment with. These proteins may go nowhere and be deleted from the genome over time, but they may also serve a valuable purpose and stay permanently established in the genome.
Vakirlis says that “there could be a lot more” SORFs that haven’t been found yet, and that some of them could cause disease. He says, “These are only tests on two cell lines,” and he adds that future tests on other cell lines might give a lot of health-related information. “We could start thinking about how to use sORFs as therapeutic targets,” he says.