Abstract. The rapidly intensifying process of ocean acidification (OA) due to anthropogenic CO2 is not only depleting carbonate ions necessary for calcification but also causing acidosis and disrupting internal pH homeostasis in several marine organisms. These negative consequences of OA on marine calcifiers, i.e. oyster species, have been very well documented in recent studies; however, the consequences of reduced or impaired calcification on the end-product, shells or skeletons, still remain one of the major research gaps. Shells produced by marine organisms under OA are expected to show signs of dissolution, disorganized microstructure and reduced mechanical properties. To bridge this knowledge gap and to test the above hypothesis, we investigated the effect of OA on juvenile shells of the commercially important oyster species, Magallana angulata, at ecologically and climatically relevant OA levels (using pH 8.1, 7.8, 7.5, 7.2). In lower pH conditions, a drop of shell hardness and stiffness was revealed by nanoindentation tests, while an evident porous internal microstructure was detected by scanning electron microscopy. Crystallographic orientation, on the other hand, showed no significant difference with decreasing pH using electron back-scattered diffraction (EBSD). These results indicate the porous internal microstructure may be the cause of the reduction in shell hardness and stiffness. The overall decrease of shell density observed from micro-computed tomography analysis indicates the porous internal microstructure may run through the shell, thus inevitably limiting the effectiveness of the shell's defensive function. This study shows the potential deterioration of oyster shells induced by OA, especially in their early life stage. This knowledge is critical to estimate the survival and production of edible oysters in the future ocean.

Autonomous endogenous time-keeping is ubiquitous across many living organisms, known as the circadian clock when it has a period of about 24 h. Interestingly, the fundamental design principle with a network of interconnected negative and positive feedback loops is conserved through evolution, although the molecular components differ. Filamentous fungus Neurospora crassa is a well-established chrono-genetics model organism to investigate the underlying mechanisms. The core negative feedback loop of the clock of Neurospora is composed of the transcription activator White Collar Complex (WCC) (heterodimer of WC1 and WC2) and the inhibitory element called FFC complex, which is made of FRQ (Frequency protein), FRH (Frequency interacting RNA Helicase) and CK1a (Casein kinase 1a). While exploring their temporal dynamics, we investigate how limit cycle oscillations arise and how molecular switches support self-sustained rhythms. We develop a mathematical model of 10 variables with 26 parameters to understand the interactions and feedback among WC1 and FFC elements in nuclear and cytoplasmic compartments. We performed control and bifurcation analysis to show that our novel model produces robust oscillations with a wild-type period of 22.5 h. Our model reveals a switch between WC1-induced transcription and FFC-assisted inactivation of WC1. Using the new model, we also study the possible mechanisms of glucose compensation. A fairly simple model with just three nonlinearities helps to elucidate clock dynamics, revealing a mechanism of rhythms’ production. The model can further be utilized to study entrainment and temperature compensation.

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