![2023 Research & Creative Achievement Day](../../../../assets/md5images/eae28255a1568fcfc3b6897dfeac6e14.png)
Abstract
Drosophila melanogaster central brain neuroblasts asymmetrically segregate proteins along the cell's apical-basal axil. Divisions along abnormal orientations or the complete failure to divide asymmetrically may result in overgrowth phenotypes. Neuroblastoma, one of the deadliest solid tumor diseases with extremely poor survival rate for late stages, is an example of this dysregulation. The protein Inscuteable (Insc) was previously found to bind with the protein Partner of Inscuteable (Pins; mPins or LGN in mammals), a receptor-independent G-protein activator, which is a subunit of the Pins-Gαi complex. The combined complex recruits Dlg to ensure correct spindle attachment on the cortex of the cell, therefore determining the orientation of the cell division. Insc was also found to bind to the protein Bazooka (Baz, Par-3) which is a subunit of the PAR-complex. This complex also contains the proteins Par-6 and aPKC. The PAR complex phosphorylate and displace cell fate determinants at the apical side of the cell, which dictate the apical-basal polarity of the cell. The two crucial complexes both interact with Insc to facilitate normal asymmetric segregation; mutation in Insc, Baz, or Pins may lead to cancer. Here we investigate the binding regions between Insc and Baz, as well as between Insc and Pins. So far, the binding sequence between Insc and Pins has been narrowed down to Insc amino acids 301-331. Further mutations will be done in this region to determine and narrow the binding sequence for all 4-protein binding sites. After determining the binding sequences between both complex interactions with Insc, point mutation will be introduced to healthy drosophila neuroblast (WT) and phenotype will be determined via the quantification of neuroblast numbers in mutant animals.
College
College of Science & Engineering
Department
Chemistry
Campus
Winona
First Advisor/Mentor
Jonathon Mauser
Start Date
4-19-2023 9:00 AM
End Date
4-19-2023 10:00 AM
Presentation Type
Poster Session
Format of Presentation or Performance
In-Person
Session
1a=9am-10am
Poster Number
30
Included in
Investigations of the Effects of Mutations in Inscuteable Mediated Pins-Mud Complex and PAR Complex Functions in Drosophila Neuroblast
Drosophila melanogaster central brain neuroblasts asymmetrically segregate proteins along the cell's apical-basal axil. Divisions along abnormal orientations or the complete failure to divide asymmetrically may result in overgrowth phenotypes. Neuroblastoma, one of the deadliest solid tumor diseases with extremely poor survival rate for late stages, is an example of this dysregulation. The protein Inscuteable (Insc) was previously found to bind with the protein Partner of Inscuteable (Pins; mPins or LGN in mammals), a receptor-independent G-protein activator, which is a subunit of the Pins-Gαi complex. The combined complex recruits Dlg to ensure correct spindle attachment on the cortex of the cell, therefore determining the orientation of the cell division. Insc was also found to bind to the protein Bazooka (Baz, Par-3) which is a subunit of the PAR-complex. This complex also contains the proteins Par-6 and aPKC. The PAR complex phosphorylate and displace cell fate determinants at the apical side of the cell, which dictate the apical-basal polarity of the cell. The two crucial complexes both interact with Insc to facilitate normal asymmetric segregation; mutation in Insc, Baz, or Pins may lead to cancer. Here we investigate the binding regions between Insc and Baz, as well as between Insc and Pins. So far, the binding sequence between Insc and Pins has been narrowed down to Insc amino acids 301-331. Further mutations will be done in this region to determine and narrow the binding sequence for all 4-protein binding sites. After determining the binding sequences between both complex interactions with Insc, point mutation will be introduced to healthy drosophila neuroblast (WT) and phenotype will be determined via the quantification of neuroblast numbers in mutant animals.