Expression of Sam-S^GD1486 under the control of Scer\GAL4^esg-NP5130 together for tubGal80[ts] to bypass the developmental stage or with also the Scer\GAL80^Su(H).GBE added for intestinal stem cell-specific knock-down, results in significantly reduced number of proliferating (EdU+) cells in the adult midgut.

Interestingly, expression of Sam-S^GD1486 under the control of an enterocyte driver, Scer\GAL4^{Myo31DF-NP0001} (and tub-Gal80[ts]), results in a marked increase in the number of EdU-positive cells as well as mitotic pH3-positive in the posterior midgut and this does not appear to be a compensation mechanism for excessive cell loss as the level of apoptosis is not increased. However, this increase in the number of proliferating cells is not observed when the knock-down is driven by the combination of both the Scer\GAL4^{Myo31DF-NP0001} and the Scer\GAL4^esg-NP5130 driver (with tub-Gal80[ts]).

Adults expressing Sam-S^GD1486 under the control of Scer\GAL4^elav.PLu (in the presence of Dcr-2^Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.

Expression under the control of Scer\GAL4^Mef2.PR results in late pupal lethality.

Expression under the control of Scer\GAL4^pnr-MD237 results in bristle morphology defects on the notum in 10-20% of the Scer\GAL4^pnr-MD237 expression domain.

Expression under the control of Scer\GAL4^pnr-MD237 results in the absence of 90-100% of the Scer\GAL4^pnr-MD237-expressing area of the notum.