What the Pandemic Experience Taught Us About STEM Higher Education-School Partnerships.

The move to virtual schooling and other measures to reduce the spread of SARS-CoV-2 infection dramatically changed the educational experience for grades K-12 populations during the years 2020 and 2021. STEM teaching and learning, and community partnerships focused on STEM education, were not exempt from the changes. Universities and other community partners had to adapt their STEM partnership programming to address new needs and assist students, teachers, families, and schools throughout periods of at-home learning and the re-reintroduction of in-person classes. Some of the changes included developing new programs, providing health-related guidance to school leaders, and converting student-focused programs to virtual formats. Through these experiences, new approaches emerged and lessons were learned that can be applied to partnership activities during normal times. These lessons included recognizing the importance of addressing inequities in students' access to technology; development of strategies to redesign enrichment programs and classroom instruction for effective online delivery; and identifying and adapting to the range of technologies available to support virtual teaching in differing schools. The increased familiarity by all partners with virtual formats has opened the door to greater participation by students in STEM enrichment programs, online partnerships with STEM professionals and mentoring opportunities.

Genetic variants related to disease susceptibility and immunotolerance in the Duffy antigen receptor for chemokines (DARC, Fy) gene in the black lion tamarin (Leontopithecus chrysopygus, primates).

The DARC (Duffy antigen receptor for chemokines) gene encodes the DARC protein, which serves multiple roles in the immune system, as a binding site for the malarial parasites Plasmodium vivax and Plasmodium knowlesi, a promiscuous chemokine receptor and a blood group antigen. Variation in DARC may play particularly significant roles in innate immunity, immunotolerance and pathogen entry in callitrichines, such as the black lion tamarin (Leontopithecus chrysopygus). We compared amino acid sequences of DARC in the black lion tamarin (BLT) to non-human Haplorhine primates and Homo sapiens. Consistent with prior studies in other Haplorhines, we observed that the chemokine receptor experiences two opposing selection forces: (1) positive selection on the Plasmodium binding site and (2) purifying selection. We observed also that D21N, F22L, and V25L differentiated BLT from humans at a critical site for P. vivax and P. knowlesi binding. One amino acid residue, F22L, was subject to both positive selection and fixation in New World monkeys, suggesting a beneficial role as an adaptive barrier to Plasmodium entry. Unlike in humans, we observed no variation in DARC among BLTs, suggesting that the protein does not play a role in immunotolerance. In addition, lion tamarins differed from humans at the blood compatibility Fya /Fyb antigen-binding site 44, as well as at the putative destabilizing residues A61, T68, A187, and L215, further supporting a difference in the functional role of DARC in these primates compared with humans. Further research is needed to determine whether changes in the Plasmodium and Fya /Fyb antigen-binding sites disrupt DARC function in callitrichines.

Variation in the flowering time orthologs BrFLC and BrSOC1 in a natural population of Brassica rapa.

Understanding the genetic basis of natural phenotypic variation is of great importance, particularly since selection can act on this variation to cause evolution. We examined expression and allelic variation in candidate flowering time loci in Brassica rapa plants derived from a natural population and showing a broad range in the timing of first flowering. The loci of interest were orthologs of the Arabidopsis genes FLC and SOC1 (BrFLC and BrSOC1, respectively), which in Arabidopsis play a central role in the flowering time regulatory network, with FLC repressing and SOC1 promoting flowering. In B. rapa, there are four copies of FLC and three of SOC1. Plants were grown in controlled conditions in the lab. Comparisons were made between plants that flowered the earliest and latest, with the difference in average flowering time between these groups ∼30 days. As expected, we found that total expression of BrSOC1 paralogs was significantly greater in early than in late flowering plants. Paralog-specific primers showed that expression was greater in early flowering plants in the BrSOC1 paralogs Br004928, Br00393 and Br009324, although the difference was not significant in Br009324. Thus expression of at least 2 of the 3 BrSOC1 orthologs is consistent with their predicted role in flowering time in this natural population. Sequences of the promoter regions of the BrSOC1 orthologs were variable, but there was no association between allelic variation at these loci and flowering time variation. For the BrFLC orthologs, expression varied over time, but did not differ between the early and late flowering plants. The coding regions, promoter regions and introns of these genes were generally invariant. Thus the BrFLC orthologs do not appear to influence flowering time in this population. Overall, the results suggest that even for a trait like flowering time that is controlled by a very well described genetic regulatory network, understanding the underlying genetic basis of natural variation in such a quantitative trait is challenging.

An introduction to a novel population genetic approach for HIV characterization.

The rapid evolution of the HIV genome is influenced in part by host selection pressure, which may cause parallel evolution among strains under shared selection pressures. To understand the mechanisms behind HIV-host immune escape across host populations, researchers have compared signatures of positive selection pressure on HIV codons across HIV subtypes and across phylogenetic groups of isolates within major subtypes, all relying on a criterion of phylogenetic separation. The HIV codon sites that retain diversity, evolve convergently among sets of hosts (cohorts) and diverge between cohorts may be phylogenetically undiagnostic (reveal little information about the relationship of the strains) and thus undetectable on a tree. We propose a new approach to characterizing genetic divergence among isolates using existing population genetic methods to better understand HIV response to host selection pressures. The approach combines population genetic statistical methods with codon analysis to identify putative amino acid sites evolving convergently. To illustrate the approach, we compared the C2-V3-C3 region of the envelope protein of HIV-1 clade B isolates between Haiti and USA hosts. This region showed no phylogenetic separation between host populations. Still, we identified codon sites in the C2-V3-C3 HIV-1 region that may have evolved differently between the two host populations. The sites are localized in human leukocyte antigen (HLA) class I binding epitopes, N-glycosylation motifs or both and are limited to the C2 and C3 regions. Our method provides a potential means to reveal candidate sites actively involved in HIV-1 immune escape that would otherwise be missed if a requisite for phylogenetic distinctiveness was made a priori. This strategy may prove to be a helpful way to characterize HIV genetic variation among hosts with suspected selection pressure differences, like progressors versus non-progressors.

Tuberculosis is associated with a down-modulatory lung immune response that impairs Th1-type immunity.

Immune mediators associated with human tuberculosis (TB) remain poorly defined. This study quantified levels of lung immune mediator gene expression at the time of diagnosis and during anti-TB treatment using cells obtained by induced sputum. Upon comparison to patients with other infectious lung diseases and volunteers, active pulmonary TB cases expressed significantly higher levels of mediators that counteract Th1-type and innate immunity. Despite the concomitant heightened levels of Th1-type mediators, immune activation may be rendered ineffectual by high levels of intracellular (SOCS and IRAK-M) and extracellular (IL-10 and TGF-betaRII, IL-1Rn, and IDO) immune suppressive mediators. These modulators are a direct response to Mycobacterium tuberculosis as, by day 30 of anti-TB treatment, many suppressive factors declined to that of controls whereas most Th1-type and innate immune mediators rose above pretreatment levels. Challenge of human immune cells with M. tuberculosis in vitro up-regulated these immune modulators as well. The observed low levels of NO synthase-2 produced by alveolar macrophages at TB diagnosis, along with the heightened amounts of suppressive mediators, support the conclusion that M. tuberculosis actively promotes down-modulatory mediators to counteract Th1-type and innate immunity as an immunopathological strategy. Our data highlight the potential application of immune mediators as surrogate markers for TB diagnosis or treatment response.