. Author manuscript; available in PMC: 2008 Oct 7.

Published in final edited form as: Biochim Biophys Acta. 2006 Oct 18;1772(4):446–456. doi: 10.1016/j.bbadis.2006.10.007

Table 2.

TOR-signaling mediators tested for modification of tau-induced neurodegeneration phenotypes

TOR signaling mediator	System^*	Interaction with tau^**
TOR^LOF	Ret	Sup
Rheb^LOF	Ret	Sup
S6k^LOF	Ret	Sup
eIF4e^LOF	Ret	Sup
UAS-4ebp^GOF	Ret	None
UAS-Tsc1	Ret	Sup
UAS-Tsc2	Ret	Sup
UAS-Tsc2^GOF	Ret	Sup
UAS-TOR	Ret	None^***
UAS-Rheb	Ret, Br	Enh (Ret), Lethal (Br)
UAS-Tsc2^LOF	Ret	Enh

Retina (Ret; driver: GMR-GAL4), Brain (Br; driver: elav-GAL4)

^**

Synergistic Enhancement (Enh), Suppression (Sup) of tau-induced neurodegeneration, No effect (None), Lethal combination when co-expressed (Lethal).

^***

Overexpression of TOR is known to paradoxically cause a loss-of-function phenotype during development [102]. Overexpression of the Rheb GTPase, however, activates the pathway [99, 100].

Abbreviations: Dominant negative (DN), Loss-of-function allele (LOF), Gain-of-function/constitutively active allele (GOF); UAS (Upstream Activating Sequence) refers to GAL4-responsive transgenes.

Bold face indicate unexpected interactions.

Information regarding specific genetic reagents is published [46], or is available from the authors by request.