Submission Title

Testing the Response of a Sensor of Silencing to a Defect in Target Message Deadenylation

Location

Jereld R. Nicholson Library

Subject Area

Biology

Description

The CCR4-NOT deadenylation complex is a group of proteins that function together to control gene expression. The Drosophila homolog for NOT2, a subunit of the CCR4-NOT complex, was identified in a forward genetic screen that identified flies defective for microRNA (miRNA) mediated gene silencing. Flies lacking functional NOT2 fail to silence our GFP-based reporter of miRNA mediated gene silencing, however the specific role of NOT2 in gene silencing is unclear. We aim to determine whether deadenylation activity of the CCR4-NOT complex, which is carried out by POP2, is essential for silencing our reporter. To address this question we are generating flies that lack functional POP2 and contain our reporter of miRNA silencing activity. If we observe that POP2 mutants fail to silence the reporter of silencing, we can infer that deadenylation activity of the CCR4-NOT complex is essential for the silencing of our reporter. However, if POP2 mutants silence the reporter, we can infer that NOT2 silences the reporter in a manner independent of deadenylation.

This document is currently not available here.

Share

Import Event to Google Calendar

COinS
 
May 15th, 9:30 AM May 15th, 10:45 AM

Testing the Response of a Sensor of Silencing to a Defect in Target Message Deadenylation

Jereld R. Nicholson Library

The CCR4-NOT deadenylation complex is a group of proteins that function together to control gene expression. The Drosophila homolog for NOT2, a subunit of the CCR4-NOT complex, was identified in a forward genetic screen that identified flies defective for microRNA (miRNA) mediated gene silencing. Flies lacking functional NOT2 fail to silence our GFP-based reporter of miRNA mediated gene silencing, however the specific role of NOT2 in gene silencing is unclear. We aim to determine whether deadenylation activity of the CCR4-NOT complex, which is carried out by POP2, is essential for silencing our reporter. To address this question we are generating flies that lack functional POP2 and contain our reporter of miRNA silencing activity. If we observe that POP2 mutants fail to silence the reporter of silencing, we can infer that deadenylation activity of the CCR4-NOT complex is essential for the silencing of our reporter. However, if POP2 mutants silence the reporter, we can infer that NOT2 silences the reporter in a manner independent of deadenylation.