09-P013 Birth of the Fin Bud

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MECHANISMS OF DEVELOPMENT

metabolic labeling of nascent rRNA transcripts was performed with

1 2 6 (2 0 0 9) S1 5 1–S 18 1

09-P012 – Withdrawn

32

P-orthophosphate. sycorax embryos show strong accumu-

lation of rRNA precursors and a decrease in 18S and 28S rRNA species, suggesting a defect in processing. In mammals, disruption of ribosome biogenesis leads to

09-P013

nucleolar stress and induction of apoptosis through activation

Birth of the Fin Bud

of the tumour suppressor, p53. To investigate whether the defects

Heiner Grandel, Michael Brand

in rRNA processing in sycoraxs845 mutants result in p53 upregulation, quantitative RT-PCR was performed. Markedly increased lev-

Biotec and CRTD, University of Technology, Dresden, Germany

els of p53, cyclinG1 and p21 mRNAs were observed. We hypothesize that the sycorax mutation results in abnormal TFIIH complex formation and/or regulation, causing abnormal RNA polymerase I mediated transcription and rRNA processing defects. We are currently exploring the mechanisms linking the rRNA processing defects in sycorax with the tissue-specific nature of its developmental abnormalities.

The vertebrate limb bud has the capacity to autonomously organize the development of an appendage, mediated through the action of signalling centers that reside in the bud itself. Analysis and cloning of zebrafish fin mutants has considerably advanced our understanding of the genetic interactions that lead to fin bud and organizer formation. Yet the initial event of limb field specification has turned out remarkably resistant to investigation.

doi:10.1016/j.mod.2009.06.340

During our analysis of the contribution of retinoic acid (RA) to fin development we have found that RA acts at different stages. Based on the analysis of the no fin mutant, that blocks 09-P011

the RA biosynthetic pathway, and on pharmacological inhibi-

Novel signals guiding endodermal progenitor cells toward a

tion of RARs, we have suggested that fin field specification is

pancreatic fate

initiated during gastrulation and that RA signalling is a neces1

1

2

Kristin Petzold , Heike Naumann , Ali H. Brivanlou , 1

Francesca M. Spagnoli

sary component of this process [Grandel etal., Development 129, 2851ff]. Difficulties about this conclusion have remained, however,

1

Max-Delbrueck-Center, Berlin, Germany

2

The Rockefeller University, New York, United States

because of the late read outs used for fin induction. We therefore search for markers of the presumptive lateral plate mesoderm that show RA dependence of this tissue already during gastrula-

Commitment of endodermal cells to pancreatic fate occurs as

tion. We find such genes and our results point to an effect of RA

a multistep process that eventually leads to the activation of the

signalling on hypoblast patterning at midgastrula stages. We

pancreatic gene expression program. While much is known about

can thus show RA dependence of pattern formation in the pec-

how the pancreas undergoes differentiation, growth and morpho-

toral fin forming tissue at a much earlier time than previously

genesis, we know little about early pancreatic specification.

shown.

In previous studies using the Xenopus system, we identified the signaling factor Shirin as a novel molecular player acting in the

doi:10.1016/j.mod.2009.06.343

time window between endoderm specification and initiation of pancreas development. The Xenopus gene shows high similarity to a unique human RhoGAP gene, named DLC2. Very little is known about the biological function of this protein and, in partic-

09-P014 – Withdrawn

ular, no embryological function has been assigned to it in mammalian species. Here, we show that Shirin is specifically expressed in the endoderm and future pancreatic rudiments from gastrulation onwards both in frog and mouse embryos, representing one the earliest markers of the pancreatic endoderm. Gain-offunction experiments performed in Xenopus indicated that Shirin alone is sufficient to induce pancreatic identity in the embryo, acting as a pancreatic instructive factor. In line with this, we observe

09-P015 Oct4 controls apical ectodermal ridge integrity and function during limb bud development Ana Raquel Toms1,2, Yolanda Gan Presmanes1, Adriana Lzaro Domnguez1, Joaquin Rodrguez-Len1,2

defects in pancreas formation upon conditional ablation of Shirin

1

gene expression in the mouse pancreatic endoderm. In particular,

Extremadura, Badajoz, Spain

Shirin conditional knockout mouse exhibits severe pancreatic

2

hypoplasia, possibly due to a reduction in number of specified

Oeiras, Portugal

Dpto. Anatomia, Biologia Celular y Zoologia Fac. Medicina, Univ. Centro Biologia de Desenvolvimento, Instituto Gulbenkian de Cincia,

pancreatic progenitors. Taken together, the gene expression profile and functional studies suggest a conserved role for Shirin at

Patterning of organs during development is controlled by the

the very early stages of the cascade of events leading to the spec-

activity of specialized groups of cells called organising centres.

ification of vertebrate pancreatic fate.

The apical ectodermal ridge (AER) is the center that controls proximo-distal outgrowth during limb development. This specialized

doi:10.1016/j.mod.2009.06.341

thickening of ectodermal cells at the tip of the limb bud is responsible for maintaining the underlying mesenchymal cells in an