Course-based undergraduate research experiences (CUREs) provide students opportunities to engage in research in a course. Aspects of CURE design, such as providing students opportunities to make discoveries, collaborate, engage in relevant work, and iterate to solve problems are thought to contribute to outcome achievement in CUREs. Yet how each of these elements contributes to specific outcomes is largely unexplored. This lack of understanding is problematic, because we may unintentionally underemphasize important aspects of CURE design that allow for achievement of highly valued outcomes when designing or teaching our courses. In this work, we take a qualitative approach and leverage unique circumstances in two offerings of a CURE to investigate how these design elements influence outcome achievement. One offering experienced many research challenges that increased engagement in iteration. This level of research challenge ultimately prevented achievement of predefined research goals. In the other offering, students experienced fewer research challenges and ultimately achieved predefined research goals. Our results suggest that, when students encounter research challenges and engage in iteration, they have the potential to increase their ability to navigate scientific obstacles. In addition, our results suggest roles for collaboration and autonomy, or directing one’s own work, in outcome achievement.

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Highlights d Disruption of SHOU4/4L genes suppresses mutants with decreased cellulose d shou4 shou4l mutants have increased levels of amorphous cellulose d SHOU4/4L are novel plant proteins that interact with cellulose synthases (CESAs) d SHOU4 proteins negatively regulate CESA exocytosis

The plant cell wall is a highly dynamic structure that changes in response to both environmental and developmental cues. It plays important roles throughout plant growth and development in determining the orientation and extent of cell expansion, providing structural support and acting as a barrier to pathogens. Despite the importance of the cell wall, the signaling pathways regulating its function are not well understood. Two partially redundant leucine-rich-repeat receptor-like kinases (LRR-RLKs), FEI1 and FEI2, regulate cell wall function in Arabidopsis thaliana roots; disruption of the FEIs results in short, swollen roots as a result of decreased cellulose synthesis. We screened for suppressors of this swollen root phenotype and identified two mutations in the putative mitochondrial pyruvate dehydrogenase E1α homolog, IAA-Alanine Resistant 4 (IAR4). Mutations in IAR4 were shown previously to disrupt auxin homeostasis and lead to reduced auxin function. We show that mutations in IAR4 suppress a subset of the fei1 fei2 phenotypes. Consistent with the hypothesis that the suppression of fei1 fei2 by iar4 is the result of reduced auxin function, disruption of the WEI8 and TAR2 genes, which decreases auxin biosynthesis, also suppresses fei1 fei2. In addition, iar4 suppresses the root swelling and accumulation of ectopic lignin phenotypes of other cell wall mutants, including procuste and cobra. Further, iar4 mutants display decreased sensitivity to the cellulose biosynthesis inhibitor isoxaben. These results establish a role for IAR4 in the regulation of cell wall function and provide evidence of crosstalk between the cell wall and auxin during cell expansion in the root.

Sucrose-specific regulation of gene expression is recognized as an important signaling response, distinct from glucose, which serves to modulate plant growth, metabolism, and physiology. The Arabidopsis MYB transcription factor Production of Anthocyanin Pigment-1 (PAP1) plays a key role in anthocyanin biosynthesis and expression of PAP1 is known to be regulated by sucrose. Sucrose treatment of Arabidopsis seedlings led to a 20-fold induction of PAP1 transcript, which represented a 6-fold increase over levels in glucose-treated seedlings. The PAP1 promoter was not sufficient for conferring a sucrose response to a reporter gene and did not correctly report expression of PAP1 in plants. Although we identified 3 putative sucrose response elements in the PAP1 gene, none were found to be necessary for this response. Using deletion analysis, we identified a 90 bp sequence within intron 1 of PAP1 that is necessary for the sucrose response. This sequence was sufficient for conferring a sucrose response to a minimal promoter: luciferase reporter when present in multiple copies upstream of the promoter. This work lays the foundation for dissecting the sucrose signaling pathway of PAP1 and contributes to understanding the interplay between sucrose signaling, anthocyanin biosynthesis, and stress responses.