Year of Publication

2007

Document Type

Thesis

College

Arts and Sciences

Department

Biology

First Advisor

Douglas A. Harrison

Abstract

The duration and intensity of the JAK/stat signaling must be tightly regulated to prevent excessive transcriptional response and to reset the pathway to receive additional signals. Socs are the largest class of these regulators in mammals. Eight Socs genes have been found in mammals. CIS, and SOCS1-3, the canonical Socs, are transcriptionally activated by and down-regulate the JAK signaling. Socs4-7, the non-canonical Socs, are less studied and their relationship with the JAK/STAT pathway has not been well established. The Drosophila genome encodes three non-canonical Socs homologues, Socs16D, Socs36E, and Socs44A. Expression of Socs36E is controlled by the JAK pathway and misexpression causes phenotypes similar to that from reduction of JAK in both ovary and wing, which may make it functionally more similar to the canonical Socs. Expression of Socs44A is not controlled by the JAK pathway and misexpression causes JAK mutant phenotypes in wing but not in ovary. Imprecise excision mutants of the three Socs genes have been generated by us and have no visible phenotypes. The mutants of Socs36E and Socs44A significantly enhance the tumor formation in hopTum-l mutant, a gain-of-function mutation of the JAK/STAT pathway. The function of Drosophila Socs will be further studied with different strategies.

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