Abstracts - Society for Developmental Biology

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Fgfr3 expression in the limb chondrocytes. Characterizing the pug mutant and defining the in vivo function of Xylt1 will
greatly enhance our understanding of the signaling pathways and factors that coordinate skeletogenesis.
Program/Abstract # 83
BMP heterodimer signaling in the developing vertebrate embryo
Mullins, Mary; Dutko, James A. Perelman Sch of Med At Univ of Penn Cell & Developmental Biology, Philadelphia,
United States
The vertebrate embryonic dorsoventral (DV) axis is patterned by a bone morphogenetic protein (BMP) activity gradient.
The BMP morphogen gradient is shaped primarily by the movement of BMP antagonists emanating from dorsal regions to
ventral regions of the embryo. High BMP signaling levels arise ventrally whereas BMP antagonists attenuate signaling
dorsally. In the zebrafish embryo, BMP signaling requires two ligands, Bmp2b and Bmp7a, functioning exclusively as a
heterodimer, and their corresponding type I receptors, Alk3/6 and Alk8 (Alk2 paralog). Why BMP heterodimers function
as the obligate ligand, while BMP homodimers, although present, fail to signal is an unanswered question and fundamental
to the BMP signaling mechanism. Here we test one model for the obligatory function of BMP heterodimers in DV
patterning: BMP antagonists preferentially block signaling by BMP homodimers. To test this model, we depleted Chordin,
Noggin1, and Follistatin-like1b by injecting translation blocking morpholinos into bmp7a or bmp2b mutant embryos,
i.e.,embryos devoid of BMP heterodimers. If BMP antagonists preferentially block signaling by BMP homodimers over
heterodimers in vivo then we expect BMP homodimers to restore signaling when BMP antagonists are removed.
Interestingly, no rescue was observed in embryos lacking BMP antagonists and BMP heterodimers. Thus, BMP
heterodimers prevail during DV patterning by a mechanism other than a preferential block to BMP homodimers by BMP
antagonists. We are currently investigating alternative hypotheses for the exclusive function of BMP heterodimers in DV
patterning, including that BMP heterodimers bind to the receptor complex with a lower overall dissociation constant
compared to BMP homodimers.
Program/Abstract # 84
acal is a novel negative regulator of Drosophila JNK signaling during embryonic dorsal closure.
Rios-Barrera, L. Daniel, Universidad Nacional Autonoma de Mexico (UNAM), Juriquilla, Mexico; Riesgo-Escovar, Juan
R. (UNAM, Queretaro, Mexico)
Dorsal closure is one of the last major morphogenetic rearrangements taking place during Drosophila embryogenesis. It
consists of the stretching of the lateral epidermis towards the dorsal midline, and is controlled by the JNK signaling
pathway. The only Drosophila JNK (encoded by basket) is activated at the most dorsal row of epidermal cells, from where
it coordinates cell remodeling by inducing cytoskeleton modifications and signaling to adjacent cells. Mutants for JNK
pathway genes die harboring a ‘dorsal open’ phenotype in cuticle preparations. In this work, we characterize a novel
‘dorsal open’ group gene, which we named acal. We generated an allelic series of acal mutants and mapped them to a nonannotated
transcript with a low in silico protein coding capacity. We hypothesize that this transcript is a microRNA
precursor. This contention is supported by high throughput RNA-sequencing by the modENCODE project. We also found
that the transcript is enriched in nuclear preparations as expected for a nucleus-processed RNA. To get insight into the role
of acal in JNK signaling, we analyzed genetic interactions of acal with basket mutants, and observed that basket mutations
rescue acal defects. Similarly, JNK signaling target genes are ectopically expressed in acal mutants. These results show
that Acal counteracts JNK signaling. acal is expressed in the epidermis, and its expression pattern is very similar to that of
raw, another negative regulator of JNK signaling. Interestingly, acal expression is reduced in raw mutants, suggesting that
Raw may act at least partially through Acal to downregulate JNK signaling during dorsal closure.
Program/Abstract # 85
Notch controls daughter cell proliferation in Drosophila neural lineages
Bivik, Caroline, Linkoping University, Linköping, Sweden
While tremendous progress has been made with respect to the mechanisms controlling neural diversification, less is known
regarding how the precise cell number of each neural sub-type is generated. The Drosophila embryonic CNS has been a
valuable model for addressing these issues. The fly CNS is generated by a set of 1,000 progenitor cells, denoted
neuroblasts, which form in the early embryo. Neuroblasts undergo repetitive rounds of asymmetric divisions, budding off
daughter cells, before exiting the cell cycle after a distinct number of divisions. In most, if not all, early stages of lineage
development, daughter cells divide once to generate two neurons/glia (Type I behavior). Recently, it has been
demonstrated that some lineages display a proliferation switch, such that late-born daughters differentiate directly into
neurons/glia (Type 0 behavior). As a consequence of these precise proliferation decisions each particular neuroblast
generates a stereotyped lineage tree and lineage size. Thus, development of a lineage depends upon two fundamental