Category:MichSt14A 9

Figure 2: Shows both that slNAC1 is expressed more in the leaves than other parts of the plant (more susceptible to desiccation) and that it is expressed more under drought conditions.

Figure 5: Shows that slNAC1 expressing plants recovered from drought and continued to grow and produce seeds while non-slNAC1 expressing plants generally died.

Fig 4: Uses a yeast-one-hybrid screen to reveal that only transformants containing the slNAC1 gene were able to grow on a medium without His, Trp or Ade. Furthermore, only these transformants showed beta-galactosidase activity indicating transcription activation. To further support these results, Fig 3 uses a GFP protein construct to show that slNAC1 is localized in the nucleus.

Figure 7a shows that in comparison with the wild type, a mutated Nce102 gene causes actin mislocalization. Fig 7b shows that the cells were also more round that the wild type which can indicate an actin defect

Figure 5: Shows that GmPTF1 is located in the nucleus

Figure 6: Used yeast clones and beta-galactosidase assays to show that the N-terminal and C-terminal domains of the full GmPTF1 are used to activate transcription. Only when both are functional can the reporter genes for Ade, Ura and his be activated Figure 7: Shows via qRT-PCR that GmPTF1 expression was induced in soybean varieties more tolerant to phosphate starvation. Time point sampling of plant organs showed that phosphate starvation induced the expression in the tolerant plants. This shows that GmPTF1 is likely a transcription factor involved in phosphate starvation response.

Fig 3: Uses agar colony growth as well as qRT-PCR descriptions of the amount of lafK, a swarming regulator gene, to shows that in comparison with cells expressing LuxT, those with the gene knocked out have decreased swarming ability and general motility.

Figure 3a: Shows that LuxT positively regulates the productions of extracellular protease (characterized endotoxins). This was detected using gene mutants and a HPA coloration assay to detect the extracellular protease levels.

Figure 3b: Includes a western blot that shows extracellular protease production is markedly decreased in a LuxT knockout. These results indicate that LuxT positively regulated extracellular protease production which further indicates that LuxT regulates endotoxin activity.

Figure 2

Fig 4: Shows that certain groups of NPR3 mutants which have decreased expression have decreased lesion sizes when inoculated with pathogenic bacteria.

Fig 5: Shows that in transgenic plants designed to express or not express NPR3, NPR3 expressing plants are less resistant to pathogenic lesions.