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Riemer, P.

Publications and source records attributed to Riemer, P..

3 recordsLinked to original sources

Testing the peak-end rule in bumblebees: lack of preference for a higher-reward sequence when the final reward is disappointing

The peak-end rule describes the tendency to evaluate experiences by their most intense and final moments, rather than considering the entire experience as a whole. While this cognitive bias is well-established in humans, studies on nonhuman animals are very limited. Bumblebees make foraging decisions largely based on past experiences, but whether peak-end effects influence their subsequent flower choices is still unknown. Here, we trained individual Bombus terrestris workers on two artificial flower types, alternating blue and yellow, over 12 consecutive foraging bouts. One flower type offered a sequence of three high-quality rewards (25 L drops of 50% w/w sucrose solution: "consistent" sequence), while the other provided the same sequence but ended with an additional, lower-quality reward (25 L drop of 20% w/w sucrose solution: "poor end" sequence). We then tested the bees flower type preference in a final binary choice. Bees showed a strong preference for blue flowers, both in their initial and overall visits. Across all visits during a 1-minute period, they also favoured flowers associated with the "consistent" sequence, though this preference was significant only when these flowers were yellow. Interestingly, despite offering more sucrose per foraging bout, bees did not favour the "poor end" sequence flower. This study is, to our knowledge, the first to investigate peak-end effects in an insect. How bees evaluate sequential rewards when foraging remains largely unexplored, yet could provide valuable insights into nectar distribution and plant-pollinator co-evolution.

animal behavior and cognition↗

An Integrative Genetic, Epigenetic and Proteomic Characterization of Pancreatic Neuroendocrine Neoplasms (PanNENs) defines Distinct Molecular Features of α- and β-cell like Subgroups

Pancreatic Neuroendocrine Carcinomas (PanNECs) are high-grade, poorly-differentiated tumors grouped together with Pancreatic Neuroendocrine Tumors (PanNETs) and placed within the Pancreatic Neuroendocrine Neoplasms (PanNENs) WHO tumor classification. Despite recent studies suggesting the endocrine origin of low-grade PanNETs, high-grade PanNEC origin remains unknown. DNA methylation analysis using the Illumina 850K beadchip array was conducted on 57 PanNEN samples, including 14 PanNECs. Distinct methylation profiles separated PanNEN samples into two major groups, clearly distinguishing high-grade PanNECs from other PanNETs including high-grade NETG3. DNA mutations, copy number changes and Immunohistochemistry of pancreatic cell-type markers PDX1, ARX and SOX9 were utilized to further characterize PanNECs and their hierarchical cell of origin in the pancreas. Phylo-epigenetic and cell-type signature features using methylation data from normal alpha, beta, acinar and ductal adult cells indicate an exocrine cell of origin for PanNECs, thus separating them in cell lineage from other PanNENs of endocrine origin. Our study provides a robust and clinically relevant method relying on methylation profiles to clearly distinguish PanNECs from PanNETG3s to improve patient stratification and treatment.

cancer biology↗

Cell type-dependent differential activation of ERK by oncogenic KRAS or BRAF in the mouse intestinal epithelium

Mutations activating the KRAS GTPase or the BRAF kinase are frequent in colorectal cancer and are thought to constitutively activate the terminal mitogen-activated protein kinase, ERK. Using mass cytometry, we found graded phosphorylation of ERK anti-correlated with cell differentiation in patient-derived colorectal cancer organoids, independent of KRAS mutational status. Reporter, single cell transcriptome and mass cytometry analyses showed that transgenic KRASG12V activated ERK in a cell type-specific pattern in mouse intestinal organoids. In contrast, transgenic BRAFV600E triggered high ERK activity and downstream gene expression in all intestinal cell types, followed by epithelial disorganisation. Quantitative network modelling from perturbation data revealed that activation of ERK is shaped by cell type-specific MEK to ERK feed forward and negative feedback signalling. We identified dual-specificity phosphatases as candidate modulators of ERK activity between intestinal cell types. Furthermore, we found that oncogenic KRAS, together with {beta}-Catenin, favoured expansion of crypt cells with high ERK activity. Our experiments highlight key differences between ERK activity elicited by the BRAF or KRAS oncogenes in colorectal cancer and find unexpected heterogeneity in a signalling pathway with fundamental relevance for cancer therapy.

cell biology↗