CoccoChannel

Context Biomineralising organisms have developed unique cellular mechanisms to control crystal growth. There is huge interest in exploiting these abilities to generate sustainable nanomaterials for biotechnological applications. Coccolithophores set the standard for precision bioengineering due to their remarkable ability to generate intricate crystal morphologies. Coccolith production by these marine algae plays a critical role in the global carbon cycle and occurs entirely intracellularly, enabling precise control of calcite morphology at nanoscale resolution. However, this process requires highly specialised cellular mechanisms that remain poorly understood. Challenge Precision engineering of calcite crystal growth by coccolithophores requires tight regulation of cellular ion transport to deliver substrates (calcium and bicarbonate) and remove excess H+. To exploit calcification for biomimetic approaches, we need to understand how these ion fluxes are controlled and identify the individual molecular mechanisms responsible. Advance Coccolithophores use voltage-gated H+ channels (Hv) in the plasma membrane to remove excess H+ generated by calcification. We recently discovered that inhibition of Hv channels in coccolithophores leads to highly specific defects in coccolith morphology. This discovery allows us to determine for the first time how an individual molecular mechanism contributes to controlled growth of calcite crystals during coccolith formation. The nature of coccolith malformations caused by Hv channel inhibition suggests that they specifically impact the latter stages of coccolith development. This has led us to propose a new model for ion fluxes during coccolith formation. We hypothesise that calcification rate is not constant throughout coccolith formation but increases as the individual crystals grow in size, leading to a greater requirement for Hv channels as the coccolith develops. Aims We aim to identify the specific role of Hv channels in the regulation of crystal growth during coccolith formation. We will use single cell physiology approaches to measure H+ fluxes throughout coccolith maturation and determine the contribution of Hv channels to cellular pH homeostasis. These will be combined with high-resolution imaging approaches to identify the specific aspects of crystal morphology that become disrupted. We propose that Hv channels play a specific role in alleviating the massive intracellular H+ load associated with crystal growth in the latter stages of coccolith formation. Objectives WP1) To determine how calcification rates and ionic fluxes change within single cells during coccolith formation. WP2) To determine whether the role of Hv channels is linked to specific stages of coccolith maturation WP3) To determine how manipulation of calcification rate influences cellular H+ load and the requirement for Hv channels WP4) To examine how functional diversification within coccolithophore Hv channels contributes to coccolith formation Applications The research will provide fundamental understanding of coccolithophore biomineralisation by outlining a novel mechanistic framework for the regulation of ion fluxes during coccolith formation. Our research will enable biomimetic applications seeking to control crystal growth in synthetic systems. Improved control of crystal growth will facilitate novel approaches in biomedical engineering such as delivery of drugs and cell therapies, as well as bio-inspired nanomaterials exploiting the photonic properties of calcite crystals. The research will also inform us on the cellular response of coccolithophores to a changing climate. Coccolithophores are the most abundant calcifying organisms in our oceans and are strongly threatened by changes in ocean pH caused by anthropogenic carbon dioxide emissions. Improved understanding of their mechanisms of pH homeostasis will have wide reaching environmental implications.