Macroalgal deep genomics illuminate multiple paths to aquatic, photosynthetic multicellularity.

Macroalgae are multicellular, aquatic autotrophs that play vital roles in global climate maintenance and have diverse applications in biotechnology and eco-engineering, which are directly linked to their multicellularity phenotypes. However, their genomic diversity and the evolutionary mechanisms underlying multicellularity in these organisms remain uncharacterized. In this study, we sequenced 110 macroalgal genomes from diverse climates and phyla, and identified key genomic features that distinguish them from their microalgal relatives. Genes for cell adhesion, extracellular matrix formation, cell polarity, transport, and cell differentiation distinguish macroalgae from microalgae across all three major phyla, constituting conserved and unique gene sets supporting multicellular processes. Adhesome genes show phylum- and climate-specific expansions that may facilitate niche adaptation. Collectively, our study reveals genetic determinants of convergent and divergent evolutionary trajectories that have shaped morphological diversity in macroalgae and provides genome-wide frameworks to understand photosynthetic multicellular evolution in aquatic environments.

Loss of Motility as a Non-Lethal Mechanism for Intercolony Inhibition ("Sibling Rivalry") in Marinobacter.

Bacteria from the genus Marinobacter are ubiquitous throughout the worlds' oceans as "opportunitrophs" capable of surviving a wide range of conditions, including colonization of surfaces of marine snow and algae. To prevent too many bacteria from occupying this ecological niche simultaneously, some sort of population dependent control must be operative. Here, we show that while Marinobacter do not produce or utilize an acylhomoserine lactone (AHL)-based quorum sensing system, "sibling" colonies of many species of Marinobacter exhibit a form of non-lethal chemical communication that prevents colonies from overrunning each other's niche space. Evidence suggests that this inhibition is the result of a loss in motility for cells at the colony interfaces. Although not the signal itself, we have identified a protein, glycerophosphoryl diester phosphodiesterase, that is enriched in the inhibition zone between the spreading colonies that may be part of the overall response.