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Abstract Humans and other animals are capable of reasoning. However, there are overwhelming examples of errors or anomalies in reasoning. In two experiments, we studied if rats, like humans, estimate the conjunction of two events as more likely than each event independently, a phenomenon that has been called conjunction fallacy. In both experiments, rats learned through food reinforcement to press a lever under some cue conditions but not others. Sound B was rewarded whereas Sound A was not. However, when B was presented with the visual cue Y was not rewarded, whereas AX was rewarded (i.e., A-, AX+, B+, BY-). Both visual cues were presented in the same bulb. After training, rats received test sessions in which A and B were presented with the bulb explicitly off or occluded by a metal piece. Thus, on the occluded condition, it was ambiguous whether the trials were of the elements alone (A or B) or of the compounds (AX or BY). Rats responded on the occluded condition as if the compound cues were most likely present. The second experiment investigated if this error in probability estimation in Experiment 1, could be due to a conjunction fallacy, and if this could be attenuated by increasing the ratio of element/compound trials from the original 50-50 to 70-30 and 90-10. Only the 90-10 condition (where 90% of the training trials were of just A or just B) did not show a conjunction fallacy, though it emerged in all groups with additional training. These findings open new avenues for exploring the mechanisms behind the conjunction fallacy effect. 

ABSTRACT Gametocytes of the malaria parasite Plasmodium are taken up by the mosquito vector with an infectious blood meal, representing a critical stage for parasite transmission. Calcium-independent protein kinases (CDPKs) play key roles in calcium-mediated signaling across the complex life cycle of the parasite. We sought to understand their role in human parasite transmission from the host to the mosquito vector and thus investigated the role of the human-infective parasite Plasmodium falciparum CDPK4 in the parasite life cycle. P. falciparum cdpk4 − parasites created by targeted gene deletion showed no effect in blood stage development or gametocyte development. However, cdpk4 − parasites showed a severe defect in male gametogenesis and the emergence of flagellated male gametes. To understand the molecular underpinnings of this defect, we performed mass spectrometry-based phosphoproteomic analyses of wild-type and Plasmodium falciparum cdpk4 − late gametocyte stages to identify key CDPK4-mediated phosphorylation events that may be important for the regulation of male gametogenesis. We further employed in vitro assays to identify these putative substrates of Plasmodium falciparum CDPK4. This indicated that CDPK4 regulates male gametogenesis by directly or indirectly controlling key essential events, such as DNA replication, mRNA translation, and cell motility. Taken together, our work demonstrates that PfCDPK4 is a central kinase that regulates exflagellation and thereby is critical for parasite transmission to the mosquito vector. IMPORTANCE Transmission of the malaria parasite to the mosquito vector is critical for the completion of the sexual stage of the parasite life cycle and is dependent on the release of male gametes from the gametocyte body inside the mosquito midgut. In the present study, we demonstrate that PfCDPK4 is critical for male gametogenesis and is involved in phosphorylation of proteins essential for male gamete emergence. Targeting PfCDPK4 and its substrates may provide insights into achieving effective malaria transmission-blocking strategies.