Expression of lkb1Scer\UAS.cLa in the dorsal wing (under the control of Scer\GAL4ap-md544) results in 'bent-up' small wings.
Expression of lkb1Scer\UAS.cLa in the eye (under the control of Scer\GAL4GMR.PF) results in a small and rough eye phenotype.
Expression of lkb1Scer\UAS.cLa in the developing eye, under the control of Scer\GAL4GMR.PF does not affect neuronal differentiation.
Apoptosis induced by expression of lkb1Scer\UAS.cLa under the control of Scer\GAL4e22c, is further enhanced by butyrate treatment.
Eye-specific expression of lkb1Scer\UAS.cLa (under the control of Scer\GAL4GMR.PF) induces a slight reduction in overall eye size. This reduction becomes more severe with elevated lkb1 levels.
Dorsal tissue-specific expression of lkb1Scer\UAS.cLa (under the control of Scer\GAL4ap-md544) induces a dramatic 'bent-up' wing phenotype, in a dose-dependent manner.
Scer\GAL4Bx-MS1096-driven expression of lkb1Scer\UAS.cLa dose-dependently reduces the overall wing size.
lkb1Scer\UAS.cLa-expressing cells (generated through clonal analysis in wing imaginal discs with Scer\GAL4Scer\FRT.Act5C) expand very poorly. However, this does not cause any alterations in the bristle size.
lkb1Scer\UAS.cLa-expressing cells (generated through clonal analysis in wing imaginal discs with Scer\GAL4Bx-MS1096), while displaying a dramatic reduction in cell expansion, fail to reduce wing marginal bristle size in the adult.
Overexpression of lkb1Scer\UAS.cLa under the control of Scer\GAL4GMR.PF does not affect S-phase cell number with respect to the control tissues (as assayed with BrdU). Similarly, there is no change in the phospho-His3 staining pattern, indicating that the G2-M cel cycle transition is also unaffected. However, staining with acridine orange, which specifically labels those dying cells with disrupted membrane integrity, shows prominent death signals, compared to controls, specifically in the region of lkb1Scer\UAS.cLa. Furthermore, TUNEL staining of the eye and wing discs also confirms the existence of extensive apoptosis in the lkb1-expressing cells.
Lkb1UAS.cLa, Scer\GAL4GMR.PF has increased cell death phenotype, enhanceable by SlnEP2245, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4GMR.PF, SlnEP2245 has increased cell death phenotype, suppressible by Diap1UAS.cHa, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4GMR.PF, SlnEP2245 has increased cell death phenotype, suppressible by BacA\p35UAS.cHa, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4GMR.PF has increased cell death phenotype, suppressible by Diap1UAS.cHa, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4GMR.PF has increased cell death phenotype, suppressible by hep[+]/hepr75, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4GMR.PF has increased cell death phenotype, non-suppressible by p53Ct.GUS, Scer\GAL4GMR.PF
Lkb1UAS.cLa/Scer\GAL4hs.PB is a non-suppressor of abnormal mitotic cell cycle | larval stage phenotype of AMPKαD1
Lkb1UAS.cLa, Scer\GAL4GMR.PF has eye phenotype, enhanceable by SlnEP2245, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4ap-md544 has wing phenotype, enhanceable by SlnEP2245, Scer\GAL4ap-md544
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing phenotype, enhanceable by SlnEP2245, Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing phenotype, enhanceable by msnUAS.cSa, Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing phenotype, enhanceable by pucE69/puc[+], Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing blade phenotype, enhanceable by hepAct.UAS, Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing phenotype, enhanceable by hepAct.UAS, Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing blade phenotype, enhanceable by bskUAS.cBa, Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing phenotype, enhanceable by bskUAS.cBa, Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4Bx-MS1096 has wing blade phenotype, enhanceable by msnUAS.cSa, Scer\GAL4Bx-MS1096
Lkb1UAS.cLa, Scer\GAL4GMR.PF, SlnEP2245 has eye phenotype, suppressible by SlnRNAi.Sym.UAS, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4GMR.PF has eye phenotype, suppressible by Diap1UAS.cHa, Scer\GAL4GMR.PF
Lkb1UAS.cLa, Scer\GAL4GMR.PF, SlnEP2245 has eye phenotype, suppressible by BacA\p35UAS.cHa, Scer\GAL4GMR.PF
Down-regulation of Sln through expression of SlndsRNA.Sym.Scer\UAS in the eye dramatically suppresses the narrow eye phenotype induced by lkb1Scer\UAS.cLa and SlnEP2245 (all under the control of Scer\GAL4GMR.PF).
Down-regulation of Sln using two copies of SlndsRNA.Sym.Scer\UAS restores the reduced wing size observed through expression of lkb1Scer\UAS.cLa (under the control of Scer\GAL4Bx-MS1096).
The fraction of SNF1AD1 mitotic larval brain neuroblasts that show extreme polyploidy is not changed if the larvae are also co-expressing lkb1Scer\UAS.cLa under the control of Scer\GAL4hs.PB.
lkb1Scer\UAS.cLa-induced apoptosis is not suppressed by expression of the dominant-negative p53Ct.GUS, both under the control of Scer\GAL4GMR.PF.
lkb1Scer\UAS.cLa-induced apoptosis is completely suppressed by expression of thScer\UAS.cHa, both under the control of Scer\GAL4GMR.PF. Interestingly, even when lkb1-induced apoptosis is completely blocked by th, the BrdU and His3 staining patterns do not deviate from the wild-type patterns.
A pucE69/+ background dramatically enhances the lkb1Scer\UAS.cLa-Scer\GAL4Bx-MS1096 small wing phenotype.
Simultaneous expression of hepAct.Scer\UAS with lkb1Scer\UAS.cLa (both under the control of Scer\GAL4Bx-MS1096 strongly enhances the lkb1Scer\UAS.cLa phenotype, resulting in severe disruption in the structure and size of the wing blades.
Simultaneous expression of bskScer\UAS.cBa with lkb1Scer\UAS.cLa (both under the control of Scer\GAL4Bx-MS1096 strongly enhances the lkb1Scer\UAS.cLa phenotype, resulting in severe disruption in the structure and size of the wing blades.
Simultaneous expression of msnScer\UAS.cSa with lkb1Scer\UAS.cLa (both under the control of Scer\GAL4Bx-MS1096 strongly enhances the lkb1Scer\UAS.cLa phenotype, resulting in severe disruption in the structure and size of the wing blades.
A hepr75 mutant background suppresses JNK pathway activation normally found when lkb1Scer\UAS.cLa is expressed by either Scer\GAL4GMR.PF or Scer\GAL4ap-md544. In addition, Scer\GAL4GMR.PF>lkb1Scer\UAS.cLa-induced apoptosis in eye imaginal discs is also completely suppressed.
Dosage reduction of grim, rpr, and W genes, through the deficiency Df(3L)H99 alleviates lkb1Scer\UAS.cLa-Scer\GAL4GMR.PF-induced apoptosis.
Co-expression of BacA\p35Scer\UAS.cHa with both lkb1Scer\UAS.cLa and SlnEP2245 considerably suppresses the apoptotic cell death induced by lkb1Scer\UAS.cLa and SlnEP2245 co-expression in the eye (all under the control of Scer\GAL4GMR.PF).
Lkb1UAS.cLa is partially rescued by Scer\GAL4ap-md544/Lkb1K201I.UAS
Lkb1UAS.cLa/Scer\GAL4hs.PB rescues Lkb1X5
A partial downregulation of JNK activity by expression of kinase-dead lkb1K201I.Scer\UAS modestly rescues the adult phenotype induced by Scer\GAL4ap-md544-driven lkb1Scer\UAS.cLa expression.
Transgenic expression of lkb1Scer\UAS.cLa using a Scer\GAL4hs.PB driver successfully rescues the lethality of lkb1X5 mutants.
Ectopic expression of lkb1Scer\UAS.cLa under the control of Scer\GAL4hs.PB successfully suppresses the 'big brain' phenotype observed in lkb1X5 mutants.