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Whether to undergo genome sequencing in a clinical or research context is generally a voluntary choice. Individuals are often motivated to learn genomic information even when clinical utility—the possibility that the test could inform medical recommendations or health outcomes—is low or absent. Motivations to seek one's genomic information can be cognitive, affective, social, or mixed (e.g., cognitive and affective) in nature. These motivations are based on the perceived value of the information, specifically, itsclinicalutility andpersonalutility. We suggest that motivations to learn genomic information are no different from motivations to learn other types of personal information, including one's health status and disease risk. Here, we review behavioral science relevant to motivations that may drive engagement with genome sequencing, both in the presence of varying degrees of clinical utility and in the absence of clinical utility. Specifically, we elucidate 10 motivations that are expected to underlie decisions to undergo genome sequencing. Recognizing these motivations to learn genomic information will guide future research and ultimately help clinicians to facilitate informed decision making among individuals as genome sequencing becomes increasingly available.

In the green alga Chlamydomonas reinhardtii, regulation of the cell cycle in response to external cues is critical for survival in a changing environment. The loss of the nuclear COMPROMISED HYDROLYSIS OF TRIACYLGLYCEROLS 7 (CHT7) protein affects the expression of many genes especially in response to nitrogen availability. Cells lacking CHT7 exhibit abnormal cell morphology following nitrogen deprivation and fail to resume normal cell division after N resupply. To investigate the function of CHT7 in the regulation of cell cycle-related pathways, cells were synchronized, and RNA-seq analysis was performed during various stages of the cell cycle. In the cht7 mutant following nitrogen deprivation, the cells were not dividing, but a subset of cell cycle genes involved in DNA replication and mitosis were found to be derepressed, suggesting that the CHT7 protein plays a role in cell cycle regulation that is opposite to that of the mitotic cyclin-dependent kinases. Furthermore, genes for cell wall synthesis and remodeling were found to be abnormally induced in nondividing cht7 cells; this misregulation may deplete cellular resources and thus contribute to cell death following nitrogen deprivation. Lastly, 43 minimally characterized kinases were found to be highly misregulated in cht7. Further analysis suggested that some of these CHT7-regulated kinases may be related to the MAP3K and Aurora-like kinases, while others are unique. Together, these results suggest a role of CHT7 in transcriptional regulation of the cell cycle and reveal several pathways and genes whose expression appears to be subject to a CHT7-mediated regulatory network.