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Congress Abstracts - Society for Developmental Biology

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Program/Abstract # 1<br />

Mechanical <strong>for</strong>ce controls chemical signals in creating plant pattern<br />

Elliot Meyerowitz (Caltech, USA)<br />

One pattern generated by the stem cells at the tip of each plant shoot – the shoot apical meristem – of flowering plants has held a<br />

fascination <strong>for</strong> generations of biologists and mathematicians. This is the phyllotactic pattern, the pattern of leaves and flowers around<br />

the stem. The most common such pattern is the spiral phyllotactic pattern, which creates the highly recognizable organization of<br />

compound fruits such as pineapples, of flowers like roses, and of inflorescences such as sunflowers. The model plant Arabidopsis<br />

thaliana also has a spiral phyllotaxis, and we have used genetic, genomic, and cell biological approaches to learn in detail how the<br />

cells of the meristem collaborate to generate this pattern. The major chemical signal is auxin, which has a specific transport system, in<br />

which a family of plasma membrane proteins directs the efflux of the hormone from cells. The efflux proteins are not uni<strong>for</strong>mly<br />

distributed, thereby causing efflux directionally, leading to a net flow of auxin in complex patterns across the surface of the meristem.<br />

Auxin not only induces new primordia of leaves and flowers, but also changes the physical properties of the cell wall. These physical<br />

changes alter the stress pattern in the meristem surface, which in turn regulates the position of the auxin efflux carrier in<br />

anisotropically stressed cells. The feedback between auxin concentration and physical stress creates the dynamic auxin patterns that<br />

cause successive auxin peaks at positions approximately 130-140 degrees around the stem, creating the spiral (and other patterns of)<br />

phyllotaxis. The stress pattern in the meristem also regulates the microtubule cytoskeleton of meristematic cells, and consequently it<br />

may also dictate the plane of cell division. The stress pattern may also determine directions of cellulose synthesis in the cell wall, and<br />

thus the subsequent direction of cellular growth, and the anisotropy of cells – leading to changes in auxin flow, and, consequently,<br />

feedbacks on the stress pattern.<br />

Program/Abstract # 2<br />

Unusual patterns of Hox cluster evolution<br />

Peter Holland, Ferdinand Marletaz, Laura Ferguson, Jordi Papas, (Ox<strong>for</strong>d, UK), Fei Xu (Chinese Academy of Science, China), Willie<br />

Taylor (NIMR, UK), Pete Olson (Nat Hist Museum London, UK)<br />

In the 1980s, the discovery of Hox gene clusters in very different animals paved the way <strong>for</strong> an integrated science in which principles<br />

and processes of embryonic development could be compared between widely divergent evolutionary lineages. A picture has emerged<br />

of a conserved Hox gene cluster pattering the ancient head-to-tail axis across all bilaterian animals. Yet there are modifications, and<br />

these differences between species may be very helpful in our attempts to link genotype evolution to phenotype evolution. Using<br />

examples from on-going research, I will discuss intriguing examples of Hox cluster breakage, Hox cluster expansion and Hox cluster<br />

shrinkage.<br />

Program/Abstract # 3<br />

Regulation of gene expression by RNA polymerase II promoter pausing during mouse embryonic development<br />

Megan Jane Wilson (Univ. of Otago, New Zealand)<br />

Proximal-promoter pausing by RNA polymerase II (RNA-polII) is a key rate-limiting step in transcription initiation. Recent genomewide<br />

studies using chromatin-immunoprecipitation to detect stalled RNA-polII have shown that promoter-pausing occurs <strong>for</strong> a number<br />

of genes, particularly developmental control genes. This stalling is believed to be a mechanism of gene regulation, causing RNA-polII<br />

to be paused near a promoter region, ready to respond to environmental or developmental cues. Two transcription elongation factors<br />

DSIF and NELF control promoter stalling by RNA-polII. Our laboratory studies sex-specific differentiation of developing mouse<br />

embryo tissues and we have utilized this system to study RNA polII stalling and its effect on gene expression over key developmental<br />

stages. Using ChIP-seq with antibodies against RNApolII, we identified many promoters that have RNA-polII stalled in a sex-specific<br />

manor in both gonad and head tissue at 13.5 dpc. This corresponded to differences in gene expression between the sexes <strong>for</strong> the<br />

associated gene transcript (as assayed by qPCR). For some transcripts, RNA polII stalling marked them <strong>for</strong> future activation at a later<br />

time point in development. In other cases, paused RNA polII was associated with genes that were becoming down regulated. This data<br />

also reveals that promoter pausing can occur differently between sexes during development. We also have preliminary evidence that<br />

indicates that components of NELF and DSIF complexes are expressed differently between the sexes during embryogenesis. Together<br />

our data suggests that some genes are being poised to respond to a signal and then strongly upregulated, whereas transcription at other<br />

genes is stalled but not activated, perhaps in the absence of an appropriate signal.<br />

Program/Abstract # 4<br />

Withdrawn<br />

Program/Abstract # 5<br />

Characterization of human developmental enhancers: from whole genomes to single SNPs<br />

Alvaro Rada Iglesias (Univ. of Cologne, Germany)<br />

Distal regulatory elements, such as enhancers, play a preponderant role in the establishment of cell-type and developmental-stage<br />

specific gene expression profiles. However, these elements are difficult to identify, since they lack strong defining features and show<br />

limited sequence conservation. In the first part of my talk, I will summarize my postdoctoral work, in which epigenomic approaches<br />

were used to characterize the enhancer repertoire of pluripotent (i.e. human embryonic stem cells (hESC)) and multipotent (i.e. human<br />

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