Congress Abstracts - Society for Developmental Biology

Ana Macias, Gimena Fussero, Carolina Arias, Marcelo Zacharonok (U Nacional de Cordoba, Argentina)
The relation among proliferation and death during growth is explained by the competition mechanism. This sees, the cells growth, in
relation with their neighbors; if the rhythms of growth are not coincidental, the lower growing cells are removed by apoptosis.There is
a special type of cell competition called morphogenetic apoptosis.This occurs if discontinuities in the growth /surviving signals
Dpp/Wg are induced.Under these circumstances death mediated by the JNK mechanism is observed at the borders of the
discontinuities. A tissue-physiologycal scenario for such discontinuities could be the time/place when Dpp and Wg expressions start.
The differences in the amount among, expressing and non expressing cells should be high at the beginning but should decreased as
development progress. In accordance, morphogenetic apoptosis must occurs at the borders of Dpp/Wg expressions. We tested this idea
in the genital disc of Drosophila where the activation of Dpp occurs late in development, there is a cell division arrest up to that time,
and death plays roles. We center our analysis in the activities of Dpp, JNK, the pro-apoptotic genes RGH and the enzymes caspases.
Our main results indicated there is cell competition/morphogenetic apoptosis at the borders of Dpp expression, revealed principally
not by the death but for its compensatory proliferation. The net balance among death/proliferation appeared cero, so physiologycal cell
competition does not vary the size. The levels of active JNK and caspases are important for: the execution of death, the control of
proliferation, and the occurrence of compensatory proliferation.The JNK/capases activity over proliferation determines them as factors
of cell competition.
Program/Abstract # 96
"Audio, Video Disco" - Establishing the cellular pattern of the organ of Corti
Andy Groves (Baylor Coll Med, USA)
The organ of Corti is a highly specialized sensory structure running along the length of the mammalian cochlear duct. It contains a
precisely organized array of mechanosensory hair cells, surrounded by glial-like supporting cells. The exquisite mechanical sensitivity
of this structure is necessary for the high frequency hearing that is a characteristic of most mammals. The almost crystalline
arrangement of cells in the organ of Corti is established by tightly orchestrated sequence of patterning signals. First, a gradient of
BMP signaling is established across the cochlear duct that positions the progenitors for the organ of Corti in the middle of the duct.
Second, local signaling centers established by this BMP gradient interact to define the boundaries of the organ of Corti progenitor
domain. For example, expression of Notch ligands and Fringe glycosyltransferases on one side of the progenitor domain set up an
asymmetrical pattern of Notch signaling that precisely defines the position and numbers of hair cells that differentiate at this boundary.
Third, FGF signaling from differentiating hair cells acts locally to precisely define the number and position of particular classes of
supporting cells. It does this by regulating transcription factors such as Hey2 that are normally considered to be targets of Notch
signaling. We speculate that this co-option of new regulatory pathways may have contributed the evolution of this highly derived
sensory organ.
Program/Abstract # 97
Role of Abdominal-B and Planar Cell Polarity in controlling Left-Right asymmetry establishment and morphogenesis in
Drosophila
Stéphane Noselli (Inst. Signal. Dev. Biol. & Cancer Res., France); Jean-Baptiste Coutelis, Charles Geminard, Nicanor Gonzalez-
Morales (Inst. de Biologie Valrose, France)
Breaking left-right (L/R) symmetry in Bilateria embryos is a major event in body plan organization. The establishment of L/R
asymmetry is essential for handedness, directional looping of internal organs (heart, gut...) and differentiation of the heart and brain.
Defects in L/R asymmetry during embryogenesis can lead to a variety of defects including congenital heart diseases, spontaneous
abortion, asplenia, polysplenia, etc. In vertebrates, L/R asymmetry can be set up at distinct embryonic stages, and involves distinct
mechanisms including the nodal flow, ions flux and asymmetric cell migration. In order to better understand how L/R asymmetry is
established, we initiated the study of L/R asymmetry in Drosophila. We identified the rotation of genitalia as a suitable L/R
phenotypic marker: during metamorphosis, genitalia undergo a stereotyped 360° clockwise (or dextral) rotation leading to the coiling
of the spermiduct around the gut. The myosinID gene (myoID, aka Myo31F) was identified as a major L/R determinant in flies,
required for dextral coiling of organs including genitalia and gut. In the absence of myoID gene activity, flies show a situs inversus
phenotype and organs undergo sinistral morphogenesis. A modifier genetic screen was performed to identify potential myoID
interacting genes during L/R patterning. We show that the Abdominal-B (Abd-B) gene controls early establishment of L/R
asymmetry, distinct from its function in anterior-posterior patterning. Abd-B mutant flies develop symmetrically, with Abd-B
controlling the expression of the myoID dextral determinant, as well as the activity of the opposite sinistral pathway. Therefore, Abd-
B acts as a symmetry breaking factor controlling the transition from symmetry to asymmetry. We will also present new results
showing how MyoID and Planar Cell Polarity control the coiling of the hindgut. We characterized a specific L/R organizer for the
adult hindgut and show that MyoID acts cell non-autonomously in this organizer to direct PCP-driven directional torsion in the
adjacent tissue. Altogether, these data provide new information on the upstream mechanisms breaking symmetry in Drosophila as well
as downstream pathways executing asymmetric morphogenesis. Publications : Adam et al., Development 2003 ; Spéder et al., Nature
2006; Hozumi et al., Nature 2006 ; Spéder & Noselli, Curr. Opin. Cell Biol. 2007 ; Spéder et al., Curr. Opin. Genet. Dev.
2007 ; Coutelis et al., Sem. Cell Dev. Biol., 2008 ; Suzanne et al., Curr. Biol. 2010 ; Petzoldt et al., Development 2012 ; Coutelis et al.,
Developmental Cell, 2013.
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