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Full Abstracts – PATTERN FORMATION
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Domain specific E3 ubiquitin ligase mediated Wingless degradation promotes Dorso-Ventral lineage in the developing
Drosophila
eye.
Meghana
Tare
1
, Madhuri Kango-Singh
1,2,3
, Amit Singh
1,2,3
. 1) Dept of Biology, Uninversity Dayton, 300 College Park Drive, Dayton OH; 2) Premedical Program,
University of Dayton, 300 College Park Drive, Dayton OH; 3) Center for Tissue Regeneration and Engineering at Dayton (TREND), University of
Dayton,300 College Park Drive, Dayton OH.
During early eye development, axial patterning transforms a single sheet of organ primordium cells to a three-dimensional organ by generating Dorso-
ventral (DV), antero-posterior (AP), and proximo-distal (PD) axes. Drosophila eye anlagen initiates with a ventral ground state on which the dorsal eye fate
is established, which requires a large number of eye specific proteins. Members of the Notch signaling pathway, Lobe (
L
; PRAS40 in vertebrates) and
Serrate (
Ser
; Jagged-1 in vertebrates), play an important role in ventral eye growth and development. Loss of function of
L
/
Ser
results in loss of ventral half
of the eye. In a genetic modifier screen,
cullin-4
(
cul-4
) was identified as a modifier of
L
mutant phenotype in the ventral eye.
cul-4
encodes an E3 ubiquitin
ligase - an enzyme that ligates ubiquitin molecules to the proteins targeted for degradation. However, the pathway through which
cul-4
exerts its effects on L
is not known. Using
Drosophila
eye as a model system, we characterized the functions of
cul4
, and its interactions with
L
using loss and gain of function
approaches. Our studies suggest that
cul-4
acts downstream of
L
, and promotes cell survival in the ventral region of the developing eye by targeting
Wingless (Wg) signaling components for degradation. Here we present a novel mechanism of DV specific ubiquitin mediated protein degradation that
promotes and maintains dorsal ventral (DV) lineage in the developing early eye field.
90
Fat and Mitochondrial Complex I component NdufV2 interact to regulate planar cell polarity.
Anson Sing
1
, Maïlis Bietenhader
2
, Lacramioara Fabian
3
,
Robyn Rosenfeld
1
, Julie Brill
3
, G Angus McQuibban
2
, Helen McNeill
1
. 1) Molecular Genetics, University of Toronto, Toronto, ON, Canada; 2) Department
of Biochemistry, University of Toronto, ON, Canada; 3) Program in Developmental & Stem Cell Biology, The Hospital for Sick Children, Toronto, ON,
Canada.
Planar cell polarity (PCP) is a form of tissue organization that is important for the proper development and function of organs. The cell adhesion molecule
Fat has been previously identified as a mediator of PCP signaling; however the mechanisms and functions by which fat effect PCP signaling remain unclear.
By yeast-2-hybrid and genetic screens we uncover NdufV2, a core component of Mitochondrial Complex I, as a Fat interactor. Depletion of NdufV2 in the
Drosophila eye and wing causes PCP defects highly reminiscent of fat hypomorphic phenotypes. We also find that NdufV2 regulates the expression of four-
jointed, the only known target of Fat signaling in PCP. Furthermore, loss of Fat or NdufV2 leads to an increase in Reactive Oxygen Species, which are
implicated as signaling molecules in diverse pathways. We also detect fragments of Fat localized in the mitochondria. These data together suggest a model
whereby cleavage and mitochondrial import of the Fat cytoplasmic domain leads to ROS-dependent signals essential for PCP.