Table 4.
Scoring rubric for formative and skills assessment of student learning based on written responses to assignment (course assignment 2 in the Supplemental Material) on Y. pestis module
| Learning objective | Demonstration of competence with the tools and skill in applying the concept/approacha | Demonstration of critical thinking and synthesis of information gained through the use of Mauve and BLASTa |
|---|---|---|
| 1. Improve student's ability to use BLAST | Did the student conduct a BLAST search of the glpD, napA, and araC genes? | Did the student correctly interpret the SNP and BLAST data and successfully assign each strain and dental pulp sample to the correct biovar? |
| 2. Be able to identify genomic islands from whole genome alignments | Did the student identify a genomic island absent from strain 91001 but present in the four pathogenic strains? | Not applicable |
| 3. Know one way to explore existing annotation for genes in a genomic island and determine whether any are involved in virulence | Did the student explore the annotations for gene products located on a genomic island that is absent from strain 91001? | Did the student formulate a hypothesis as to how the proteins encoded on this genomic island may contribute to the microorganism's virulence?b |
| 4. Be able to conduct analyses addressing conservation of genes in E. coli O157:H7 or Y. pestis strains | Did the student analyze the BLAST and Mauve results correctly to determine whether his/her assigned virulence gene is present in all five Y. pestis strains, and whether it is predicted to be functional in 91001? | Did the student successfully determine that the genetic evidence supports a Pacific trade route origin for the North American lineage? |
aTasks were scored as Yes/No unless otherwise indicated.
bStudents typically pinpointed genes implicated in iron uptake and metabolism as being potentially relevant to virulence, because bacteria require iron and exhibit tight regulation of these functions. Other positive findings included fimbrial proteins, which the students suggested were involved in adhesion to host cells. Students correctly inferred that putative phage tail proteins, antirepressors, host-specificity proteins, and transposases are unlikely to be involved in virulence. One student found a putative sulfatase and sulfatase modifier and concluded that these genes were insufficient to cause virulence because they were found in the nonpathogenic E. coli strain K12 as well.