Event Title

Analysis of Bm-daf-16b Function in Brugia malayi

Mentor 1

Dr. Kirsten Crossgrove

Location

Union Wisconsin Room

Start Date

24-4-2015 10:30 AM

End Date

24-4-2015 11:45 AM

Description

Caenorhabditis elegans is a free-living nematode whose physiology and maturation closely resemble those of Brugia malayi, a parasitic nematode that causes filariasis in its host. C. elegans go through four molt stages with the potential for an intermediate stage that responds to environmental conditions. This stage of arrested development, called dauer, is similar to the L3 infective (L3i) stage of B. malayi. Both stages affect metabolism and require environmental signaling to continue to the next stage of development. In C. elegans, the insulin/IGF-1 signaling (IIS) pathway provides direction to several gene targets to continue through the stages normally. When the IIS pathway stops signaling due to environmental cues, C. elegans enters dauer. We propose that the mechanism that causes C. elegans’ formation of dauer is similar to B. malayi’s molt into L3i. One target of the insulin signaling pathway in C. elegans is daf-16, a transcriptional regulator whose resulting proteins are instrumental in initiating and maintaining dauer formation. Bm-daf-16 is negatively regulated by insulin signaling. This means that when the insulin signaling pathway is functional, Bm-DAF-16 is not activated. B. malayi has been shown to express daf-16 during L3i, which leads us to believe that Bm-daf-16 is functionally similar to Ce-daf-16, but this has yet to be proven. There are two isoforms of Bm-daf-16, Bm-daf-16a and Bm-daf-16b; my experiments deal with Bm-daf-16b. We have amplified Bm-daf-16b from cDNA, and are currently cloning it into a mammalian expression vector. Then we will transfect mammalian cells through cell culture, and observe the cells to see if Bm-DAF-16b can activate expression of a reporter gene in an insulin signaling dependent way. This would further our hypothesis that that Bm-daf-16 is functionally similar to Ce-daf-16. Such similarities, if confirmed, could be an important discovery in the battle to prevent filariasis.

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Apr 24th, 10:30 AM Apr 24th, 11:45 AM

Analysis of Bm-daf-16b Function in Brugia malayi

Union Wisconsin Room

Caenorhabditis elegans is a free-living nematode whose physiology and maturation closely resemble those of Brugia malayi, a parasitic nematode that causes filariasis in its host. C. elegans go through four molt stages with the potential for an intermediate stage that responds to environmental conditions. This stage of arrested development, called dauer, is similar to the L3 infective (L3i) stage of B. malayi. Both stages affect metabolism and require environmental signaling to continue to the next stage of development. In C. elegans, the insulin/IGF-1 signaling (IIS) pathway provides direction to several gene targets to continue through the stages normally. When the IIS pathway stops signaling due to environmental cues, C. elegans enters dauer. We propose that the mechanism that causes C. elegans’ formation of dauer is similar to B. malayi’s molt into L3i. One target of the insulin signaling pathway in C. elegans is daf-16, a transcriptional regulator whose resulting proteins are instrumental in initiating and maintaining dauer formation. Bm-daf-16 is negatively regulated by insulin signaling. This means that when the insulin signaling pathway is functional, Bm-DAF-16 is not activated. B. malayi has been shown to express daf-16 during L3i, which leads us to believe that Bm-daf-16 is functionally similar to Ce-daf-16, but this has yet to be proven. There are two isoforms of Bm-daf-16, Bm-daf-16a and Bm-daf-16b; my experiments deal with Bm-daf-16b. We have amplified Bm-daf-16b from cDNA, and are currently cloning it into a mammalian expression vector. Then we will transfect mammalian cells through cell culture, and observe the cells to see if Bm-DAF-16b can activate expression of a reporter gene in an insulin signaling dependent way. This would further our hypothesis that that Bm-daf-16 is functionally similar to Ce-daf-16. Such similarities, if confirmed, could be an important discovery in the battle to prevent filariasis.