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In the teaching and learning events of our life, there are characters who play key roles. Teachers, mentors, relatives, novels, songs, newspaper columns, often help us understand the questions in our heads. However, we often reject them because they are messages or attitudes from older people and the generation gap does not allow us to understand them well. The times of covid-19 have us locked up at home. They alert us that precisely “elderly people” are a vulnerable group. Also, we have been asked to take care of grandparents. If we are lucky enough to have an internet connection, it seems that we can learn anything we want with just one click. This could lead us to explore only what we find attractive, easy and comfortable. With this testimony, I invite you to acknowledge on the role of the elderly in the learning of entire generations. I call for openness towards diverse voices and for the understanding that we all play a role in moving towards a more mature society.

99 GENERAL AND MISCELLANEOUS↗

Molecular pathways for learning in the single-cell Stentor coeruleus

The single-cell Stentor coeruleus contracts in response to mechanical taps but habituates and learns to ignore the taps after repeated stimulation. Here, we explored the molecular changes that occur during the formation of this cellular memory in order to improve our understanding of non-synaptic learning. We impaired cellular protein synthesis with cycloheximide and puromycin and found that, contrary to the effects of such treatments on metazoa, these drugs accelerate habituation and prolong memory retention in Stentor . Exploratory proteomic and transcriptomic analyses identified candidate proteins and genes that changed over the course of habituation and response recovery, pointing toward the regulation of Stentor learning by calcium signaling and protein phosphorylation. Building on these results, we found that using RNA interference to knock down the calcium-binding, EF-hand domain-containing protein SteCoe_6763 accelerated habituation. Furthermore, increased extracellular calcium improved Stentor learning, while treatment with kinase and phosphatase inhibitors impaired learning. In particular, KN-93, a drug known to inhibit calcium/calmodulin-dependent kinase II and voltage-gated calcium channels, decreased both the rate and extent of habituation in Stentor , similar to its effects on learning in metazoa. We also discovered that habituation memory can be maintained in progeny following cell division. Taken together, these results suggest that response recovery in Stentor requires new protein synthesis and that memory formation involves the modification of delocalized mechanoreceptors by phosphorylation and calcium signaling. This is consistent with our previous model of Stentor learning, in which habituation occurs through the inactivation of cell-surface receptors.

CaMKII↗