The expression of Tctp^HMS00701 under the control of Scer\GAL4^{SPARC-MI00329-GAL4} (and Dicer-2, for a more efficient RNAi) in the larval fat body induces defective secretion, including intracellular matrix material, as shown by the retention of both secr.GFP and Vkg.GFP. Expression under the control of Scer\GAL4^Cg.PA leads to smaller endoplasmic reticulum exit sites (Sec16.GFP) that are uncoupled from the cis-Golgi (Grasp65.RFP).

Expression of Tctp^HMS00701 RNAi under the control of either Scer\GAL4^Act5C.PU (using tub-Gal80[ts] to limit the RNAi expression to the adult stage) or the Scer\GAL4^C587 driver results in germline stem cell (GMC) differentiation defects, while expression under Scer\GAL4^{nos.UTR.T:Hsim\VP16} leads to GMC loss in adult testes.

Scer\GAL4^Cg.PA, Tctp^HMS00701 has embryonic/larval fat body | third instar larval stage phenotype, non-suppressible by Rab1^{Q70L.UASp.YFP}, Scer\GAL4^Cg.PA

Scer\GAL4^Cg.PA, Tctp^HMS00701 has extracellular matrix | third instar larval stage phenotype, non-suppressible by Rab1^{Q70L.UASp.YFP}, Scer\GAL4^Cg.PA