Nkd1 functions downstream of Axin2 to attenuate Wnt signaling.

Wnt signaling is a crucial developmental pathway involved in early development as well as stem-cell maintenance in adults and its misregulation leads to numerous diseases. Thus, understanding the regulation of this pathway becomes vitally important. Axin2 and Nkd1 are widely utilized negative feedback regulators in Wnt signaling where Axin2 functions to destabilize cytoplasmic ß-catenin, and Nkd1 functions to inhibit the nuclear localization of ß-catenin. Here, we set out to further understand how Axin2 and Nkd1 regulate Wnt signaling by creating axin2gh1/gh1, nkd1gh2/gh2 single mutants and axin2gh1/gh1;nkd1gh2/gh2 double mutant zebrafish using sgRNA/Cas9. All three Wnt regulator mutants were viable and had impaired heart looping, neuromast migration defects, and behavior abnormalities in common, but there were no signs of synergy in the axin2gh1/gh1;nkd1gh2/gh2 double mutants. Further, Wnt target gene expression by qRT-PCR and RNA-seq, and protein expression by mass spectrometry demonstrated that the double axin2gh1/gh1;nkd1gh2/gh2 mutant resembled the nkd1gh2/gh2 phenotype demonstrating that Nkd1 functions downstream of Axin2. In support of this, the data further demonstrates that Axin2 uniquely alters the properties of ß-catenin-dependent transcription having novel readouts of Wnt activity compared with nkd1gh2/gh2 or the axin2gh1/gh1;nkd1gh2/gh2 double mutant. We also investigated the sensitivity of the Wnt regulator mutants to exacerbated Wnt signaling, where the single mutants displayed characteristic heightened Wnt sensitivity, resulting in an eyeless phenotype. Surprisingly, this phenotype was rescued in the double mutant, where we speculate that cross-talk between Wnt/ß-catenin and Wnt/Planar Cell Polarity pathways could lead to altered Wnt signaling in some scenarios. Collectively, the data emphasizes both the commonality and the complexity in the feedback regulation of Wnt signaling.

Which Group Dynamics Matter: Social Predictors of Student Achievement in Team-Based Undergraduate Science Classrooms.

While group work in undergraduate science education tends to have overall benefit, less is known about the specific peer-peer dynamics that optimize learning during group interaction. The current study used peer ratings and self-reported data from 436 students enrolled in team-based undergraduate science courses (biology or chemistry) to determine group dynamics that predicted both willingness to work with peers in the future and individual achievement in the course. Results show that greater personal connection and contributions predicted willingness to work with a group member (R2biology = 0.75; R2chemistry = 0.59). While active contribution to a group predicted greater achievement, more noncontent interactions (e.g., encouragement, listening to feedback, being polite) predicted lower achievement, despite these being on-task and relevant. Additionally, having group members who were willing to continue working with a student was a positive predictor of that student's achievement regardless of course. Strikingly, students in chemistry were significantly less willing to work with women in their groups compared with men. Finally, not all forms of group conflict predict decreased achievement. These findings highlight group factors such as student behavior within the group, aspects of the group social environment, and peer support that can be targeted for optimizing undergraduate science learning.

Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2.

Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/ß-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/ß-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/ß-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/ß-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo.

Validation of oil fate and mass balance for the Deepwater Horizon oil spill: Evaluation of water column partitioning.

Model predictions of oil transport and fate for the 2010 Deepwater Horizon oil spill (Gulf of Mexico) were compared to field observations and absolute and relative concentrations of oil compounds in samples from 900 to 1400 m depth <11 km from the well. Chemical partitioning analyses using quantitative indices support a bimodal droplet size distribution model for oil released during subsea dispersant applications in June with 74% of the mass in >1 mm droplets that surfaced near the spill site within a few hours, and 1-8% as <0.13 mm microdroplets that remained below 900 m. Analyses focused on 900-1400 m depth <11 km from the well indicate there was substantial biodegradation of dissolved components, some biodegradation in microdroplets, recirculation of weathered microdroplets into the wellhead area, and marine oil snow settling from above 900 m carrying more-weathered particulate oil into the deep plume.

Oil fate and mass balance for the Deepwater Horizon oil spill.

Based on oil fate modeling of the Deepwater Horizon spill through August 2010, during June and July 2010, ~89% of the oil surfaced, ~5% entered (by dissolving or as microdroplets) the deep plume (>900 m), and ~6% dissolved and biodegraded between 900 m and 40 m. Subsea dispersant application reduced surfacing oil by ~7% and evaporation of volatiles by ~26%. By July 2011, of the total oil, ~41% evaporated, ~15% was ashore and in nearshore (<10 m) sediments, ~3% was removed by responders, ~38.4% was in the water column (partially degraded; 29% shallower and 9.4% deeper than 40 m), and ~2.6% sedimented in waters >10 m (including 1.5% after August 2010). Volatile and soluble fractions that did not evaporate biodegraded by the end of August 2010, leaving residual oil to disperse and potentially settle. Model estimates were validated by comparison to field observations of floating oil and atmospheric emissions.