Abstracts - Society for Developmental Biology

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progenitor cells that cover the surface of the embryo either stratify to form epidermis or invaginate to form hair follicles
(HFs). Dramatic morphological changes take place during the first steps of HF formation at the placode stage. Dermal cells
are recruited to form the dermal condensate that will later give rise to the dermal papilla, while overlaying epidermal cells
assume more elongated columnar morphology. Additionally, placode downgrowth is asymmetric, such that HFs grow at an
acute angle towards the anterior of the mouse. Several signaling pathways, e.g. Wnt, sonic hedgehog (Shh), and
transforming growth factor beta 2 (TGF-β2) regulate HF development, but how various pathways interact and regulate cell
cycle and cytoskeleton resulting in HF downgrowth and differentiation remains largely unknown. We use a novel
lentivirus-based in vivo gene knockdown approach to explore these fascinating questions.
Program/Abstract # 143
Mechanisms of Integrin-linked kinase modulation of hair follicle morphogenesis.
Rudkouskaya, Alena; Dagnino, Lina, University of Western Ontario, London, Canada
Integrin-linked kinase (ILK) is essential for hair follicle (HF) morphogenesis. Hair follicle development arrests at stage 4-5
in ILK-deficient epidermis. To identify the processes modulated by ILK in developing HF, we examined alterations in
factors important for HF morphogenesis in embryonic ILK-deficient epidermis. LEF1 expression in embryonic day (E)
15.5 epidermal condensates is not altered in ILK-deficient epidermis indicating that ILK is not required for initial
activation of the Wnt pathway during HF specification. In contrast, LEF1 expression decreased in ILK-deficient E17.5 hair
pegs (stage 4-5). At E17.5, sonic hedgehog (Shh) signaling participates in furthering HF development. Significantly, Gli1,
a marker and mediator of Shh signaling, is expressed in E15.5-E17.5 mutant epidermis. In contrast, in the absence of ILK
P-cadherin expression is decreased, and this is accompanied by abnormal spatial expression of E-cadherin. This suggests
that ILK is required to modulate the pathways involved in upregulation of P-cadherin in coordination with downregulation
of E-cadherin during normal HF development. ILK-deficient HFs also show aberrant laminin 511 deposition in regions
between the hair matrix and the dermal papilla. In the latter, expression of key markers, such as CD133, is also impaired.
Thus, in the absence of ILK the second wave of Wnt signaling is altered during HF formation at stage 4-5, which is
associated with alterations in E- and P-cadherin expresion and, potentially, cell-cell communication. ILK is also likely
necessary for normal interactions between the developing HF epithelium and the underlying mesenchymal cells in dermal
papilla. Supported with funds from the Canadian Institutes of Health Research.
Program/Abstract # 144
Olfactory microvillous neurons arise from the neural crest in a Sox10-dependent manner
Saxena, Ankur; Peng, Brian; Bronner, Marianne, California Institute of Technology, Pasadena, United States
Development of the vertebrate olfactory system involves a complex interplay between elements of the central and
peripheral nervous systems. Classically, the olfactory ectodermal placode has been presumed to form all olfactory sensory
neurons. In contrast, here we show that cranial neural crest is the primary source of microvillous sensory neurons within
the olfactory epithelium of zebrafish. Using photo conversion-based fate mapping and live cell tracking coupled with laser
ablation, we followed neural crest precursors in transgenic zebrafish embryos as they migrated from the neural tube to the
nasal cavity. A subset of these cells, coexpressing the transcription factors Sox10 and neurogenin1, ingressed into the
olfactory epithelium and differentiated into microvillous neurons. Loss-of-functionanalysis revealed a critical role for
Sox10 in microvillous neurogenesis. In sum, these results not only challenge the dogma regarding the origin of olfactory
sensory neurons but also provide important insights into the early events that build the nascent olfactory system.
Program/Abstract # 145
Development of gustatory papillae in the absence of Six1 and Six4.
Ikeda, Keiko, Hyogo College of Medicine, Hyogo, Japan, Suzuki, Yuko (Health Sci. Univ. Hokkaido, Hokkaido, Japan);
Kawakami, Kiyoshi (Jichi Med. Univ., Tochigi, Japan)
Six-Homeo family genes code transcription factors, and a deficiency in them leads to defects in the sensory organs. Six1
was expressed in the taste bud-bearing lingual papillae of mice, and loss of Six1 affected the development of these
gustatory papillae as previously reported. We found that embryos lacking both Six1 and Six4 showed severer abnormalities
than those lacking Six1 alone during morphogenesis of their gustatory papillae. Six4 was broadly distributed in the
epithelium of the lateral lingual swellings at embryonic day (E) 11.5, and in the tongue epithelium, mesenchyme, and
muscles at E12.5. From E14, Six4 expression pattern was similar to Six1. In the fungi form papillae, Six4 expression was
observed in the epithelium at E14-E16.5. In the circumvallate and foliate papillae, Six4 was expressed in the trench wall of
these papillae at E15.5-P0. Although Six4-deficient mice had no abnormalities, Six1/Six4-deficient mice showed distinct
morphological changes: fusion of the lateral lingual swellings was delayed, and the tongue was developed poorly. The
primordia of fungi form papillae appeared earlier than those in the wild-type or Six1-deficient mice, and the papillae