By Marta Koblańska, 16.12.2025, 12:00 Poland’s time, photo: DNA clash, Pixabay
Conflicting genes enable acquiring adaptive morphs – according to a new study from Denmark and China recently published in,, Cell Press”.
The human body comprises chemical, molecular, and morphological levels. Each of them has to work properly to maintain functionality and efficiency, and all of them undergo physical rules. Otherwise, we call a diverse phase a disease, with the exception, when physical pressure is cut off due to, for instance, a Cosmos trip. All of us, at least for now, born on Earth, have two parents and need care providers until adolescence. We also need a place to live, air to breathe, and food to sustain life. Our lives are to some extent determined by genes we carry within our body in the form of a sort of prescription for our health status, which can also be slightly modified, ruined, or repaired. Now, scientists from China and Denmark in a new research titled,, Phenotypic signatures of incomplete lineage sorting in hominids” have addressed the issue of random fixations in our DNA which can lead to incomplete lineage sorting (ILS). What is it that the sorting does not sound very friendly? Simplifying it is a kind of stamp of our prehistory, which could be either common for every human due to the shared ancestor or completely different, contradicting the gene tree with the species’ morphs expressed in our phenotype. The phenotype represents the visible part of us.
What are the consequences? According to scientists, the fixations of genes originally belonging to descendant species or species having were our ancestors were related to were up into modern humans’ DNA as incomplete. Nevertheless, we constantly share similarities with gorillas in approximately 17 percent of our genome, which is more than with chimps (approximately 96-98 percent of the human genome is identical to chimps, depending on the studied sections, but how much in the phenotype?), which are our closest living relatives. And this might be explained with the ILS – incomplete lineage sorting which, according to the scientists, represents a contradiction or can be called a,, discordance in rapidly radiating lineages” leading to a kind of misplacement between expressed morphs linked to a species and expected traits generated from the gene’s tree and its clade/roots.
ILS not only alters the phylogenetic signal across the genome but also directly influences phenotypic variation by affecting genes that contribute to specific morphological traits. Functional experiments have established causal relationships between ILS-derived genetic variation and morphological diversity, further substantiating the idea that trait evolution may not adhere strictly to the bifurcating pattern implied by a simple species tree – claim Stine Keibel Blom, Christy Anna Hipsley, Guojie Zhang.
They add, however, their (ILS – MK’s note) long generation times further exacerbate ILS by extending the period during which these polymorphisms can persist before allelic sorting is completed.
This does not imply that the incomplete sorting is not useful anymore. It is, as in line with the research, can contribute or even condition the adaptation. Humans, of course, are the only hominid species to adopt habitual bipedalism, accompanied by increased precision gripping in the hand and loss of gripping capacity in the foot. But, in particular, in childhood, we can see some remains in the process of acquiring walking skills or in the form of climbing trees. What’s interesting the ILS is associated with the population size, and this is not true only for humans. This comes from the biological rule that the larger the population size, the higher the genetic diversity. However, in line with the research calling the theory of coalescence, there may be, let’s say, bigger differences, thus increasing the likelihood of ILS in smaller populations.
In line with the study, in the human genome, 7905 genes with coding regions overlap with ILS-affected sites, while 2715 human genes comprise one amino acid – 34 percent- shared with gorilla to the exclusion of chimpanzee, and 10,492 human genes contain similar regulatory components as gorilla due to ILS.
These genes are involved in various biological pathways that serve as substrates for phenotypic variation, likely generating conflicting evolutionary signals. Indeed, research indicated that genes with more ILS-affected sites tend to have similar expression patterns between human and gorilla, for example, loci involved in pathogen interactions like the major histocompatibility complex (MHC) and ABO blood group system, according to scientists.
Simplifying our understanding of tissue, we can say that the type and function of the tissue we are made of are influenced by genetic trade-offs. These traits have evolved over millions of years in hominid species, and the direction of this evolutionary process appears to be a selection of random changes. While we can predict only a few outcomes based on our current knowledge and technological advancements, the results reflect a complex interplay of genetics and evolution.
Previous functional studies have focused on human-specific traits, revealing a wealth of similarities and differences with our closest living relatives including genetic, cellular, behavioural, musculoskeletal, and physiological modifications. These findings are often interpreted as signatures of adaptive selection to past conditions, with potential trade-offs in the modern world such as increased disease risk or osteoarthritis, conclude scientists.
Stine Keibel Blom, Christy Anna Hipsley, Guojie Zhan say that understanding the phenotypic effects of these ILS-affected sites requires a combination of multi-level data with cross-disciplinary approaches, as distinguishing between strict mammalian lineages, great apes, and humans, along with balancing sections, including the immunity loci like the MHC requires careful integration of demographic modelling with tests for selection signatures. The question of whether we want it or not remains open.
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