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The lymphatic vasculature is a blind-ended network crucial for tissue-fluid homeostasis, immune surveillance and lipid absorption from the gut. Recent evidence has proposed an entirely venous-derived mammalian lymphatic system. By contrast, here we show that cardiac lymphatic vessels in mice have a heterogeneous cellular origin, whereby formation of at least part of the cardiac lymphatic network is independent of sprouting from veins. Multiple Cre-lox-based lineage tracing revealed a potential contribution from the putative haemogenic endothelium during development, and discrete lymphatic endothelial progenitor populations were confirmed by conditional knockout of Prox1 in [Tie2.sup.+] and [Vav1.sup.+] compartments. In the adult heart, myocardial infarction promoted a significant lymphangiogenic response, which was augmented by treatment with VEGF-C, resulting in improved cardiac function. These data prompt the re-evaluation of a century-long debate on the origin of lymphatic vessels and suggest that lymphangiogenesis may represent a therapeutic target to promote cardiac repair following injury., In 1902, Florence Sabin proposed that the primary lymph sacs originate from the embryonic veins and then give rise to the entire lymphatic vasculature by sprouting and remodelling (1). An [...]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2010.06.029 Byline: Atsushi Kitajima, Naoyuki Fuse, Takako Isshiki, Fumio Matsuzaki Keywords: Neuroblast; Stem cell; Self-renewal; Differentiation; Asymmetric cell division; Polarity; Prospero; Temporal identity Abstract: Asymmetric cell division generates two daughter cells of differential gene expression and/or cell shape. Drosophila neuroblasts undergo typical asymmetric divisions with regard to both features; this is achieved by asymmetric segregation of cell fate determinants (such as Prospero) and also by asymmetric spindle formation. The loss of genes involved in these individual asymmetric processes has revealed the roles of each asymmetric feature in neurogenesis, yet little is known about the fate of the neuroblast progeny when asymmetric processes are blocked and the cells divide symmetrically. We genetically created such neuroblasts, and found that in embryos, they were initially mitotic and then gradually differentiated into neurons, frequently forming a clone of cells homogeneous in temporal identity. By contrast, larval neuroblasts with the same genotype continued to proliferate without differentiation. Our results indicate that asymmetric divisions govern lineage length and progeny fate, consequently generating neural diversity, while the progeny fate of symmetrically dividing neuroblasts depends on developmental stages, presumably reflecting differential activities of Prospero in the nucleus. Article History: Received 23 January 2010; Revised 23 June 2010; Accepted 24 June 2010

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2007.09.003 Byline: Tetsuya Shirai (a), Takeshi Yorimitsu (a), Naruto Kiritooshi (a), Fumio Matsuzaki (b), Hideki Nakagoshi (a) Keywords: Drosophila; Leg; Segment; Notch; EGFR; Planar cell polarity; dve Abstract: Segmentation plays crucial roles during morphogenesis. Drosophila legs are divided into segments along the proximal-distal axis by flexible structures called joints. Notch signaling is necessary and sufficient to promote leg growth and joint formation, and is activated in distal cells of each segment in everting prepupal leg discs. The homeobox gene defective proventriculus (dve) is expressed in regions both proximal and distal to the intersegmental folds at 4 h after puparium formation (APF). Dve-expressing region partly overlaps with the Notch-activated region, and they become a complementary pattern at 6 h APF. Interestingly, dve mutant legs resulted in extra joint formation at the center of each tarsal segment, and the forced expression of dve caused a jointless phenotype. We present evidence that Dve suppresses the potential joint-forming activity, and that Notch signaling represses Dve expression to form joints. Author Affiliation: (a) Graduate School of Natural Science and Technology, Okayama University, 3-1-1 Tsushima-naka, Okayama 700-8530, Japan (b) Laboratory for Cell Asymmetry, Center for Developmental Biology, RIKEN, Kobe, Japan Article History: Received 6 April 2007; Revised 21 August 2007; Accepted 6 September 2007

Pattern formation during animal development is often induced by extracellular signaling molecules, known as morphogens, which are secreted from localized sources. During wing development in Drosophila, Wingless (Wg) is activated by Notch signaling along the dorsal-ventral boundary of the wing imaginal disc and acts as a morphogen to organize gene expression and cell growth. Expression of wg is restricted to a narrow stripe by Wg itself, repressing its own expression in adjacent cells. This refinement of wg expression is essential for specification of the wing margin. Here, we show that a homeodomain protein, Defective proventriculus (Dve), mediates the refinement of wg expression in both the wing disc and embryonic proventriculus, where dve expression requites Wg signaling. Our results provide evidence for a feedback mechanism that establishes the wg-expressing domain through the action of a Wg-induced gene product. Key Words: Drosophila wing imaginal disc; Notch; wingless; defective proventriculus; morphogen; pattern formation.

Author(s): Tomokazu Ohshiro [1, 2]; Takako Yagami [1]; Chuan Zhang [1, 2]; Fumio Matsuzaki (corresponding author) [1, 2, 3] Cellular diversity during development arises in part from asymmetric divisions, which [...]