Abstracts - Society for Developmental Biology

147
fate, potentially acting downstream of nsy-5 to antagonize Ca 2+ channel activity by decreasing voltage across the
membrane. These results establish a novel role for BK channels in neuronal fate diversification.
Program/Abstract # 444
Sox genes in C. elegans: sox-2 role in postembryonic development
Vidal Iglesias, Berta; Hobert, Oliver, Columbia University Medical Center, New York, United States
Sox proteins are a highly conserved family of transcription factors involved in several developmental processes.
Expression of SoxB genes correlates with the commitment of cells to a neural fate; however, the relevance of SoxB
proteins in early vertebrate neurogenesis has been difficult to prove genetically due to embryonic lethality and presumed
redundant functions. The nematode C. elegans has only 5 sox genes: sox-2 and sox-3 form the SoxB group while sem-2,
sox-4 and egl-13 belong to other Sox groups. Our results show that sox-2 and sem-2 are the sox genes expressed earliest
and in a broader manner during embryogenesis, being expressed in several neuronal progenitors. sox-3, sox-4 and egl-13
are expressed in few cells during late embryogenesis, when most neurons are already born. Both sox-2 and sem-2 null
mutants are early larval lethal but do not show neuronal specification defects during embryonic development as indicated
by quantification of a panneuronal reporter. Potential redundancy or compensatory mechanisms between different sox
genes have been ruled out, strongly suggesting that sox genes are not required for specification of embryonically-derived
neurons. However, at the first larval stage there are still several blast cells that will give rise to different postembryonic
lineages, which generate several neurons amongst other cell types. Interestingly, sox-2 is expressed in many of these
progenitor cells. Using mosaic analysis we have so far identified neurons derived from two different postembryonic
lineages which fail to be generated in C. elegans sox-2 mutants. These results support the idea that postembryonic
progenitor competence is compromised in the absence of sox-2.
Program/Abstract # 445
The induction of pluripotent mesoderm from axolotl animal caps by Brachyury and BMP-4
Ferjentsik, Zoltan; Chatfield, Jodie; Johnson, Andrew, University of Nottingham School of Biology, Nottingham, United
Kingdom
We developed axolotl embryos as a model system to investigate the development of primordial germ cells (PGCs) from
pluripotent cells. Axolotls are a model for the tetrapod ancestor and so accurately represent the amphibian ancestor to
mammals. As such, they share the gene regulatory networks (GRN) that control mammalian development, including the
GRN for pluripotency. In normal development axolotl PGCs develop in a posterior mesodermal compartment that acts as a
germ cell niche. Importantly, this tissue is not conserved in Xenopus or zebrafish embryos, and so little is known about
how it is specified. We showed that forced expression of Brachyury and BMP-4 induces pluripotent mesodermal tissue that
will give rise to neural tissue, including a neural tube, in addition to PGCs, and other mesodermal cell types. In normal
development this domain is induced by FGF and BMP signalling, in the absence of Nodal signals. We refer to it as
pluripotent mesoderm, which is distinct from the typical somatic mesoderm that is induced by Nodal, and we postulate that
it is homologous to the posterior mesoderm compartment that is responsible for axial elongation in mice. Discrimination
between pluripotent mesoderm and somatic mesoderm is governed by Nanog activity, and it represents one of the earliest
cell fate decisions in vertebrate embryogenesis. We are using differential transcriptomics to identify the GRN that governs
development of this novel mesodermal tissue, and we are working to understand how FGF signalling interacts with Nanog
to control its development.
Program/Abstract # 446
FGF signaling is required for lineage restriction but not onset of primitive endoderm program in the mouse
blastocyst
Kang, Minjung; Artus, Jerome; Piliszek, Ania; Hadjantonakis, Anna-Katerina, Sloan-Kettering Institute, New York,
United States
Emergence of pluripotent epiblast (EPI) and primitive endoderm (PrE) lineages within the inner cell mass (ICM) of the
mouse blastocyst occurs in several steps involving initial co-expression of lineage-specific markers, subsequent mutuallyexclusive
marker expression and salt-and-pepper distribution of lineage-biased cells, and sorting of lineage-committed
cells into respective layers. Precisely how EPI and PrE lineage commitment occurs is not entirely clear, however
FGF/ERK signaling appears to be required. To gain insight into the role of FGF signaling we investigated the phenotype
resulting from zygotic and maternal/zygotic Fgf4. Fgf4 heterozygous blastocysts exhibited increased numbers of EPI cells
and reduced numbers of PrE cells suggesting that FGF signaling must be tightly regulated to ensure appropriate cell
numbers for each lineage. Fgf4 mutants lacked PrE entirely; their ICM comprised exclusively NANOG-expressing cells.
Notably, co-expression of EPI and PrE marker was initially established, even in the absence of FGF4. Thus, Fgf4 mutant