Evolutionary Biology Discoveries

This weekend I got an early, and very unexpected Christmas present. A buddy who lives in the US texted to say he was at Heathrow and had 24 hours in London due to a connecting flight cancelation. As a result, we got to spend the whole day together, which was a fabulous surprise. Probably the first time I was ever pleased with a flight cancelation! It got me thinking about how much human brains have evolved to handle social interactions. We are a social species. This is a fundamental characteristic and maintaining social bonds is a key function of our neural circuitry. 👉 Several regions within visual cortex are tuned to recognise faces and interpret emotional expressions. These areas respond much more strongly to faces than other complex visual stimuli like objects, houses, or scenes suggesting a strong, evolutionary pressure towards recognising other individuals. 👉 Brain regions including medial prefrontal cortex, orbitofrontal cortex, angular gyri, and precuneus are implicated in social cognition, particularly in managing social hierarchies, and predicting others' intentions and behaviours. These allows for empathy and theory of mind—the ability to understand that others have beliefs, desires, and perspectives different from one's own. 👉 Reward circuits in the brain, including the meso-limbic dopamine pathway, are highly sensitive to social interactions. I got a major dopamine rush from seeing my friend’s text and another from seeing him for the first time in several years. It seems obvious that friends are rewarding, but it only happens in social species. Most species are not social and their only relationships are either with family members or are completely transactional. As a result, social interactions do not involve reward circuitry. 👉 Even the fact that our brains enable language is a function of our social species. Language provides a form of intentional mind reading. That is, my ability to write this and your ability to read it is a way to share my thoughts with you – you are essentially reading my mind at the time I wrote this. Language, and the brain adaptation that support it, evolved to facilitate complex social interactions. The Social Brain hypothesis suggests that our brains evolved to manage complex social relationships. The size and structure of our brains, particularly the neocortex, are hypothesized to have expanded to accommodate the demands of social living.   I obviously geek on this stuff, but if you find it as interesting as I do, you’d probably enjoy Nichola Raihani's “The Social Instinct.” It’s a great read full of amazing stories and genuine insight into our social species.

The striking Nature cover this week once again highlights the power of genome sequencing across time and space to give us new insights into the history of our own species. The last continent in the world to be settled by humans was the Americas. Beringia, a land bridge that replaced the Bering Strait during the last ice age, allowed the ancestors of Indigenous Americans to travel from northeast Asia into North America. Once there, they dispersed south, settling in and adapting to dramatically different environments as they did so. Tábita Hünemeier and colleagues report whole-genome sequencing data for Indigenous populations from 8 Latin American countries, representing 28 language families. They combine these data with genomes from ancient individuals and present-day populations to explore how patterns of genetic variation evolved. They reveal evidence for at least three separate dispersals into South America as well as long-term continuity and adaptation to diverse environments. This is reflected in our cover image - it illustrates the genomic diversity of Indigenous Americans through a stylized Indigenous headdress in which the colour variations represent genetic mixing within the populations, and the three upper feathers symbolize the major migration waves that shaped the peopling of South America. Cover image: Emiliano Bellini Kelly Krause https://lnkd.in/dyUkChKu

A nuance to Maslow The question of what motivates human behavior has long intrigued psychologists. The most well-known theory is Abraham Maslow's hierarchy of needs, introduced in the mid-20th century. Maslow emphasizes the social aspects of motivation but there is growing evidence that there are other key drivers of motivation. One interesting study published last month found that a lot of our motivation comes from early humans’ ability to survive in their environment. Using network analysis, the researchers from HSE University and the London School of Hygiene and Tropical Medicine identified stable clusters of motives. The study found that human behavior is driven by 15 key motives, which can be grouped into five broad categories: environmental (Hoard, Create), physiological (Fear, Disgust, Hunger, Comfort), reproductive (Lust, Attract, Love, Nurture), psychological (Curiosity, Play), and social (Affiliate, Status, Justice). The researchers found that from an evolutionary perspective Status and Play are central to shaping behavior. The study also found that motivation changes with age—young individuals prioritize Status and Play, while older adults focus on Comfort and Fear. Gender differences also emerged, with women emphasizing Nurture and Comfort, while men were more motivated by Status and Attraction. These findings have applications in marketing, AI, and mental health by helping tailor strategies to different motivational needs. Will be interesting to see how the outcomes of this study will influence the analysis and interventions around motivation in private and business life in the next years. Research: https://lnkd.in/eF_4Dbii

Consumers perceive the same coffee differently depending on whether they buy instant powder at the supermarket or order an artisanal espresso at a café. Yet the core ingredient remains the same. This shows how powerfully framing and context influences brand perception and value.   Rather than selling features no one will really use, a brand must focus on conveying a concise yet compelling identity. The most effective brand propositions tap into just a few key evolutionary drives that motivate consumers below the level of conscious awareness. Loss aversion can encourage brand loyalty if framed properly. Feelings of anticipated regret at missing out on a limited-time offer or switching from a familiar product can also sway decisions.   Great brands artfully blend left-brain functional claims with right-brain emotional resonance. By acknowledging consumers’ irrational tendencies instead of pretending they will carefully weigh every product attribute, brands can craft more compelling identities with staying power. They must look past surface-level product characteristics and connect with the evolutionary roots of human cognition that still guide our choices today.

Today our paper was published in Nature Magazine. I’d like to start with a patient’s story: A bone marrow transplant patient's gut microbiome was devastated by chemotherapy and medications. Enterococcus faecium moved in to fill the void. And then, inside this one person's gut over just 26 days, a single piece of jumping DNA rewired metabolism. The bacterium became better at scavenging folate, which is exactly the nutrient that becomes scarce when the microbiome collapses. This was the ‘magic bullet’ E. faecium needed to dominate. This isn't an evolutionary story from millions of years ago. It happened in a patient we cared for at Stanford hospital, measurable because we now have the sequencing tools to read it. The jumping gene ISL3 has been proliferating in hospital-associated E. faecium for 30 years, quietly, and in several clinical lineages. And these elements are generating extensive structural variation: not random noise, but regulatory rewiring of genes that helps this bacterium not only survive but thrive in the environments modern medicine creates. I am very proud of co-first authors Matthew Grieshop and Aaron Behr, who led this work with rigor, patience and creativity. And I am thankful to members of the Stanford Department of Medicine BMT team and clinical microbiology team who made this work possible. Most importantly, I’m grateful to the patients, their families and the nurses who made our sample collections and this meaningful patient-driven science possible. This paper required combining global genomic surveys (~20,000 pathogen genomes), long-read sequencing of clinical isolates, and longitudinal metagenomic sequencing of patient stool, because short-read sequencing simply cannot resolve highly repetitive elements like ISL3 accurately. Measuring what actually matters required building the tools to see it. There are still many mysteries to solve: the mechanism driving ISL3 expansion, its long-term consequences, and how generalizable the folate scavenging story is. But we now know that IS elements are a contemporary evolutionary force in hospital pathogens, operating on clinical timescales, inside individual patients. The hospital is a habitat. E. faecium has been learning to live in it. Open access link to the paper in comments.

Cancer is evolution under pressure. Melanoma is one of its most aggressive expressions. All cancers begin with genetic disruption — activation of oncogenes, inactivation of tumor suppressors, loss of cell-cycle control. But melanoma adds another layer: extreme genomic instability driven largely by UV-induced DNA damage. From the general principles of cancer biology: • Oncogenic activation → In melanoma, often BRAF, NRAS, NF1 • Tumor suppressor loss → CDKN2A, PTEN, TP53 alterations • Sustained proliferation → MAPK pathway hyperactivation • Immune evasion → PD-L1 expression, T-cell exhaustion • Angiogenesis and invasion → Early metastatic competence Melanoma exemplifies how mutational burden shapes biology. Its high tumor mutational burden (TMB) makes it immunogenic — which partly explains the transformative impact of immune checkpoint inhibitors. Yet, the same genomic instability that makes melanoma visible to the immune system also drives heterogeneity and resistance: • MAPK reactivation after BRAF/MEK inhibition • Loss of antigen presentation • Adaptive resistance through microenvironment remodeling Melanoma is not simply a skin tumor. It is a dynamic ecosystem — tumor cells, immune cells, stroma, vasculature — constantly evolving. From early radial growth phase confined above the basement membrane to vertical growth phase with vascular access to distant metastasis — including brain tropism — melanoma reflects the full arc of cancer biology. The lesson is clear: Understanding signaling pathways (MAPK, PI3K/AKT), immune regulation, and clonal evolution is not theoretical — it determines whether we choose immunotherapy, targeted therapy, combinations, or neoadjuvant strategies. In melanoma, biology is destiny — unless we intercept it. #Melanoma #CancerBiology #MAPK #Immunotherapy #TumorEvolution #PrecisionOncology #TranslationalResearch

How do we use evolutionary principles to concretely map how drug resistance develops in ovarian cancer patients? New work from the lab, led by the amazing Marc Williams, published today in Springer Nature addresses this problem in ovarian cancer https://lnkd.in/ecJXRUGr. Typically, studying tumor evolution has been carried out through error prone evolutionary reconstructions from single snapshots in patients. This has limited our ability to study the problem of tracking evolution of drug resistance in ovarian cancer that almost inevitably emerges through treatments and over time in patients. To overcome these hurdles, we developed an approach called CloneSeq-SV based on single cell whole genome sequencing technology and longitudinal cell-free DNA tracking technology. Our goal was to map the growth patterns of individual clones within patients to decipher the properties of cancer cells that evade therapy. To develop our approach, we exploited clone-specific structural variants that frequently accrue in ovarian cancer genomes, using them as endogenous barcodes - clone-specific fingerprints - that could be measured and tracked in the blood of cancer patients. We arrived at three important insights: 1) significant clonal evolution occurs over the therapeutic timeline- even with standard front line chemotherapy- that prunes the complexity of clonal populations found at relapse; 2) drug resistant clones frequently harbored distinctive genomic properties such as clone-specific oncogene amplification, genome doubling and chromothripsis; 3) using single cell RNA sequencing from pre-treatment samples we mapped phenotypic states to individual clones and found that plausible drug-resistant phenotypes were already present at diagnosis. This is consistent with a model of therapy induced selective pressure acting on cancer cells that might be pre-adapted prior to any treatment. Finally, in one remarkable case example, CloneSeq-SV was able to define the evolutionary steps that led to a durable clinical response to a new targeted therapy. Might an evolution-aware approach be useful to optimize therapy for our patients more generally? Future studies would be needed to confirm this. I'm grateful for the continuing collaboration with the Gynecologic Disease Management Team under the leadership of Dr. Carol Aghajanian, MD and Dr. Nadeem Abu Rustum, Dr. Dennis Chi and #TeamOvary, the Gyn molecular lab led by Dr. Britta Weigelt, Neeman Mohibullah and her team at the Integrated Genomics Operation Core facility working with Andrew McPherson, and Claire Friedman Dmitriy Zamarin, MD PhD who were along the journey for many years in the SPECTRUM program. The work was generously funded by Break Through Cancer, the Halvorsen Center for Computational Oncology, Seidenberg Family Foundation and the Ovarian Cancer Research Alliance. We are also incredibly thankful to the patients and families who are our partners in research.

Breast cancer remains a major global health challenge1. Here, to comprehensively characterize its genomic landscape and the clinical significance of genomic characteristics, we analysed whole-genome sequences from 1,364 clinically annotated breast cancers, with transcriptome data available for most cases. Our study expands the repertoire of oncogenic alterations and identifies novel driver genes, recurrent gene fusions, structural variants and copy number alterations. Timing analyses on copy number alterations suggest that genomic instability emerges decades before tumour diagnosis, and offer insights into early initiation of tumorigenesis. Pattern-driven genomic features, including mutational signatures2, homologous recombination deficiency3, tumour mutational burden and tumour heterogeneity scores4, were associated with clinical outcomes, highlighting their potential utility as predictive biomarkers for clinical evaluation of treatments such as CDK4/6 and HER2 inhibitors, as well as adjuvant and neoadjuvant chemotherapy. These findings highlight the power of large-scale, clinically annotated whole-genome sequencing in advancing our understanding of how genomic alterations shape patient outcomes. Paper and research by @Ryul Kim and larger team at Inocras Inc.

Same Brain.  Different Jungle! People aren’t underperforming because they lack talent. Their environment may be working against their brains. The noise everywhere is not helping. Escalating global tensions. Political polarisation. AI disruption. Economic volatility. Social pressure. It’s relentless. And it’s doing something very specific to the human brain. After two decades working at the intersection of psychology, neuroscience and organisational performance, one thing has become impossible to ignore. We cannot solve modern leadership challenges without understanding the brain — what it’s good at, and what it was never designed to handle. The brain evolved to survive short-term physical threats in small tribes. Our neurobiology, forged in environments of scarcity and immediacy, is superb at rapid prediction and threat detection. It is far less well equipped for chronic psychological stress, digital overload, endless change and complex organisational politics. Yet this is the jungle we now inhabit. Corporate language like ‘change management’, ‘feedback’, ‘restructuring’ and even ‘strategy’ may sound neutral.  To the brain they often signal uncertainty, status evaluation and potential loss of control. In other words, we are living through a profound evolutionary mismatch. And when the brain senses threat, performance shifts fast: - Focus narrows - Creativity drops - Collaboration weakens - Risk appetite shrinks - Cognitive capacity degrades The result? A defensive, siloed, exhausted workforce But here’s the good news. The brain is plastic. Neural pathways are not fixed; they are continually shaped by experience and environment. We can’t rewrite our evolutionary inheritance — but we can influence how it expresses itself. The implication for leaders is clear.... If the brain is constantly scanning for threat, then clarity, fairness and predictability are not ‘nice to haves’ — they are performance drivers.  That means: Communicating with clarity Framing change carefully Designing fair processes Ensuring safety Providing appropriate autonomy Culture isn’t abstract. It’s neurobiological. Every meeting, message and decision either amplifies threat or enables performance. Design the environment wisely, and the biology follows. So I’m starting something new. I will be publishing short pieces that connect: • What’s happening in the world • What neuroscience is teaching us • What leaders can do to help their people think better, feel better and perform at their best If there’s a global issue you’d like explored through a neuroscience lens, drop it in the comments. Let’s start with the brain — and take it from there!

The Structural History of Eukarya For decades, comparative genomics has relied primarily on sequence markers of single genes. Yet sequence diverges rapidly and variably between genes, often obscuring the deeper signals that encode evolutionary history. Today, we move beyond single genetic sequences. We are proud to introduce the Structural History of Eukarya (SHE): the first proteome-scale phylogeny constructed entirely from 3D protein structure. To build this new map of life, our team undertook an unprecedented computational effort: nearly 300 trillion structural alignments across 1,542 eukaryotic proteomes. By analysing evolution through global protein architecture rather than local sequence, we reveal patterns that remain invisible to traditional genomics. Key insights from SHE: 🐁 Data-driven model selection Beyond reconstructing evolutionary history, SHE is a practical resource. With valuable input from M. Madan Babu, we developed a search engine enabling researchers to quantitatively rank model organisms by their structural fidelity to specific human pathways, transforming model selection from intuition into data-driven science. 🧬 A bipartite evolutionary mode The eukaryotic cell is not a uniform molecular landscape. Instead, we resolve a deeply conserved Architectural Core that stabilises cellular organisation, supporting a highly plastic Operational Engine of metabolism and translation that drives adaptation. 🕊️ Intrinsic structural acceleration We identify lineage-specific bursts of structural innovation in groups such as Birds and Ants, demonstrating that structural evolutionary tempo can diverge markedly from simple genomic expansion. This project represents a major collaborative effort from my fantastic team Qiuzhen Li and Diandra Daumiller who did a fantastic job driving this work to completion at SciLifeLab and Stockholm University! The preprint is now available on bioRxiv, and the full dataset can be explored via our interactive server - try it to rank your model organism! 📄 BioRxiv preprint: https://lnkd.in/dvmSG-iF 🖥️ Interactive server: https://lnkd.in/dXapbNS7 Big thanks to Google DeepMind (AlphaFoldDB). Martin Steinegger (MMseqs, FoldComp, Foldseek). SciLifeLab (Web server) and M. Madan Babu (Model organism selection).