Marko Kaksonen

@kaksonen.bsky.social

Biologist fascinated by cells, molecules and the evolution of cellular processes. Membrane traffic, cytoskeleton, microscopy, fungi, evolutionary cell biology. https://www.unige.ch/sciences/biochimie/labs/marko-kaksonen/

I am starting my lab at the University of Geneva next January! Incredibly excited to soon be joining the MOCEL department as an Asst. Professor. The lab will use evolutionary cell biology to study chromosomes, centromeres & speciation 🧬🔬🌱 Intrigued, want to join or collaborate? 🔗 helsenlab.org

Helsen lab | chromosome and centromere evolution

The Helsen lab at the University of Geneva explores how centromeres and chromosomes evolve, diversify, and function across eukaryotes. Discover our latest publications, research team, and open positio...

helsenlab.org

Our new paper was, by definition, an adventure: stepping outside of our comfort zone, embracing the unknown, and engaging in activities where the outcome is uncertain. Includes discovery of a new species and working with a Native American tribe to name it… 🧵👇 onlinelibrary.wiley.com/doi/10.1002/...

Comparative Analysis of Stress Adaptation in the Yeast Microbiome of Cactus

Yeasts and related fungi isolated from cacti or nearby non-cactus plants were characterized phenotypically and genomically, revealing differences that hint at modes of adaptation to the cactus host.

onlinelibrary.wiley.com

Just got a notice of award for an R01. I will be hiring. I'll be looking for either a staff scientist or postdoctoral researcher. The project explores the conserved HEATR5 family of proteins. Their roles in AP1 mediated traffic, and links to motors.🎉

Expansion microscopy is revolutionary but application to actin cytoskeleton has been challenging. Not anymore....we combine IntAct + U-ExM to get an unprecedented 3D nanoscale view of actin isoforms in expanded cells. Read the full revised paper here: plos.io/4vansgr

IntAct-U-ExM enables super-resolution imaging of isoform-specific actin networks across species

A previous study in PLOS Biology developed IntAct, a tool to study isoform-specific actin localization, dynamics and molecular interactions across species. In this Update Article, IntAct is coupled wi...

plos.io

Saravanan Palani@syncellbiolab.bsky.social · 2mo ago

Our new paper in @plosbiology.org introduces IntAct-U-ExM enabling isoform-specific imaging of actin at nanoscale across yeast, mammalian cells & primary neurons. Fabulous work spearheaded by @anubhavdhar.bsky.social along with an amazing team! #actin #U-ExM journals.plos.org/plosbiology/...

1/35 New preprint! We show that obligate multicellularity removes fundamental population genetic barriers to multicellular adaptation. Even a brief unicellular phase can dramatically constrain the evolution of beneficial multicellular traits. www.biorxiv.org/content/10.6...

Obligate multicellularity circumvents population genetic barriers to collective-level adaptation

Complex multicellularity has evolved in just five lineages (animals, plants, brown algae, red algae, and fungi) and in each case, these organisms develop clonally and are obligately multicellular. While prior work has shown that clonal development plays a critical role in the evolution of complex multicellularity, none has disentangled this from the impact of obligate vs facultative multicellular life cycles. Here we use experimental evolution with engineered snowflake yeast ( Saccharomyces cerevisiae ) to directly test how life cycle structure affects multicellular adaptation. We created isogenic strains capable of switching between unicellular and clonal multicellular phases, then evolved populations for 192 days under obligately multicellular, facultatively multicellular, and obligately unicellular regimes. Obligately multicellular populations rapidly evolved larger size, primarily driven by a whole genome duplication, in all five replicates. Facultative populations showed dramatically constrained evolution, with tetraploidy evolving in only 2/10 facultative populations despite experiments demonstrating that it is strongly beneficial across the full life cycle. Mathematical modeling reveals the mechanistic basis for this constraint: facultative life cycles create establishment barriers through two population genetic effects. Group formation dramatically reduces the number of units of selection, making beneficial multicellular mutations vulnerable to drift. This asymmetry in population size between life cycle phases also allows cell-level selection to overpower group-level selection, eliminating mutations that provide group-level benefits but carry cell-level costs. These findings demonstrate that obligate multicellularity circumvents fundamental population genetic barriers to collective-level adaptation, helping explain why complex multicellularity has evolved exclusively in obligately multicellular lineages, and suggesting similar constraints may operate in other evolutionary transitions in individuality. ### Competing Interest Statement The authors have declared no competing interest. U.S. National Science Foundation, https://ror.org/021nxhr62, DEB-1845363 Howard Hughes Medical Institute Gilliam Fellowship National Science Foundation Graduate Research Fellowship

biorxiv.org

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