Research on Naegleria’s actin-based, microtubule-independent motility published in the Journal of Cell Biology.
- by Lillian Fritz-Laylin
- in News
- posted September 22, 2020
Dr. Katrina Velle has published her fascinating work on Naegleria gruberi’s crawling motility in a paper “Conserved actin machinery drives microtubule-independent motility and phagocytosis in Naegleria” in the Journal of Cell Biology. Lacking interphase microtubules as an amoeba, N. gruberi, related to the “brain-eating amoeba” N. fowleri, moves using conserved actin machinery despite having diverged from humans >1 billion years ago. N. gruberi can provide a great way to study “actin in a vacuum” as Katrina phrases it, studying actin phenotypes similar to those in humans without the crosstalk between the actin and microtubule cytoskeleton seen in other model systems.
Here’s the abstract: Much of our understanding of actin-driven phenotypes in eukaryotes has come from the “yeast-to-human” opisthokont lineage and the related amoebozoa. Outside of these groups lies the genus Naegleria, which shared a common ancestor with humans >1 billion years ago and includes the “brain-eating amoeba.” Unlike nearly all other known eukaryotic cells, Naegleria amoebae lack interphase microtubules; this suggests that actin alone drives phenotypes like cell crawling and phagocytosis. Naegleria therefore represents a powerful system to probe actin-driven functions in the absence of microtubules, yet surprisingly little is known about its actin cytoskeleton. Using genomic analysis, microscopy, and molecular perturbations, we show that Naegleria encodes conserved actin nucleators and builds Arp2/3–dependent lamellar protrusions. These protrusions correlate with the capacity to migrate and eat bacteria. Because human cells also use Arp2/3–dependent lamellar protrusions for motility and phagocytosis, this work supports an evolutionarily ancient origin for these processes and establishes Naegleria as a natural model system for studying microtubule-independent cytoskeletal phenotypes