|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
|
Fig. 3. Cytoplasmic activated Akt controls Lsd2 expression and specific
IIS-dependent functions. (A,B) Perilipin homologue LSD2 (B,
blue) is expressed relatively homogeneously in the nurse cell cytoplasm, which
is stained for lipid with Nile Red (A, red). (C-I) Nile Red-positive
droplets (red; arrows) in Pten-mutant (GFP-negative cell in E-I; I,H
are magnified views of anterior nurse cell in E) and
Dp110-overexpressing (C,D) nurse cells exclude the perilipin
homologue LSD2. In G,H, Nile Red is also detected in the green channel in
intensely stained large lipid droplets. LSD2 levels are highly elevated in
Pten mutant cells (F,I); normal perilipin levels are not visible at
this low imaging sensitivity. There is evidence for elevated LSD2 accumulation
around some lipid droplets (arrow in H). Arrowhead in I points to a region in
the mutant cell that does not contain LSD2 - which is presumably the nucleus.
(J) Schematic showing the established InR/PI3-kinase/Akt signalling
cassette, involving InR-dependent activation of cell-surface Akt (orange), a
process antagonized by PTEN. Our data reveal a role for cytoplasmic activated
Akt (pink) in regulating the accumulation of large lipid droplets (red) in
Drosophila nurse cells via a mechanism that, in part, involves LSD2.
Note potential negative-feedback mechanisms (green), which might be controlled
by cytoplasmic as well as surface P-Akt, and could therefore induce
differential sensitivity to insulin in different subcellular domains. Scale
bars: 40 µm.
|
