Programmed cell death (PCD) is an irreversible, genetically controlled form of cell suicide that is essential to promote and maintain genetic stability and is critical for the regulation of cellular and tissue homeostasis in metazoans. PCD has been observed in a variety of unicellular organisms including prokaryotic bloom-forming cyanobacteria, chlorophytes, dinoflagellates, diatoms, and coccolithophores. Trichodesmium also displays autocatalytic PCD in response to stressors such as oxidation, high irradiance, and Fe-depletion.
In the oceans Trichodesmium forms extensive blooms in nutrient-poor tropical and subtropical regions. These massive blooms generally collapse several days after forming, but the cellular mechanism responsible along with the magnitude of associated C and N export, are as yet unknown. Our work from laboratory simulations demonstrate that extremely rapid development and abrupt, PCD-induced demise (within 2-3 d) of Trichodesmium blooms lead to greatly elevated excretions of transparent exopolymers and a massive downward pulse of particulate organic matter. Our results mechanistically link autocatalytic PCD and bloom collapse to quantitative C and N export fluxes and suggest that PCD may impact biological pump efficiency in the oceans.