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Abstract

Although vertebrates seem to be essentially bilaterally symmetrical on the exterior, there are numerous interior left-right asymmetries in the disposition and placement of internal organs. These asymmetries are established during embryogenesis by complex epigenetic and genetic cascades. Recent studies in a range of model organisms have made important progress in understanding how this laterality information is generated and conveyed to large regions of the embryo. Both commonalities and divergences are emerging in the mechanisms that different vertebrates use in left-right axis specification. Recent evidence also provides intriguing links between the establishment of left-right asymmetries and the symmetrical elongation of the anterior-posterior axis.

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A series of normal stages in the development of the chick embryo

Viktor Hamburger, Howard L. Hamilton (1951)

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Randomization of left-right asymmetry due to loss of nodal cilia generating leftward flow of extraembryonic fluid in mice lacking KIF3B motor protein.

Shigenori Nonaka, Yosuke Tanaka, Yasushi Okada … (1998)

Microtubule-dependent motor, murine KIF3B, was disrupted by gene targeting. The null mutants did not survive beyond midgestation, exhibiting growth retardation, pericardial sac ballooning, and neural tube disorganization. Prominently, the left-right asymmetry was randomized in the heart loop and the direction of embryonic turning. lefty-2 expression was either bilateral or absent. Furthermore, the node lacked monocilia while the basal bodies were present. Immunocytochemistry revealed KIF3B localization in wild-type nodal cilia. Video microscopy showed that these cilia were motile and generated a leftward flow. These data suggest that KIF3B is essential for the left-right determination through intraciliary transportation of materials for ciliogenesis of motile primary cilia that could produce a gradient of putative morphogen along the left-right axis in the node.

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Cilia and Hedgehog responsiveness in the mouse.

Danwei Huangfu, Kathryn Anderson (2005)

The intraflagellar transport (IFT) proteins Ift172/Wimple and Polaris/Ift88 and the anterograde IFT motor kinesin-II are required for the production and maintenance of cilia. These proteins are also required for the activation of targets of the mouse Hedgehog (Hh) pathway by Gli transcription factors. The phenotypes of the IFT mutants, however, are not identical to mutants that lack Smoothened (Smo), an essential activator of the Hh pathway. We show here that mouse embryos that lack both Ift172 and Smo are identical to Ift172 single mutants, which indicates that Ift172 acts downstream of Smo. Ift172 mutants have a weaker neural patterning phenotype than Smo mutants, because Ift172, but not Smo, is required for proteolytic processing of Gli3 to its repressor form. Dnchc2 and Kif3a, essential subunits of the retrograde and anterograde IFT motors, are also required for both formation of Gli activator and proteolytic processing of Gli3. As a result, IFT mutants display a loss of Hh signaling phenotype in the neural tube, where Gli activators play the major role in pattern formation, and a gain of Hh signaling phenotype in the limb, where Gli3 repressor plays the major role. Because both anterograde and retrograde IFT are essential for positive and negative responses to Hh, and because cilia are present on Hh responsive cells, it is likely that cilia act as organelles that are required for all activity of the mouse Hh pathway.

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PubMed ID:: 16543932

DOI:: 10.1038/nrg1830

ScienceOpen disciplines: Chemistry

Keywords: Animals,Body Patterning,Embryo, Mammalian,physiology,Embryo, Nonmammalian,Embryonic Development,Nodal Protein,Transforming Growth Factor beta,metabolism,Vertebrates,embryology,genetics

Left-right asymmetry in the vertebrate embryo: from early information to higher-level integration.

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A Sustainable Future

Most cited references 77

A series of normal stages in the development of the chick embryo

Randomization of left-right asymmetry due to loss of nodal cilia generating leftward flow of extraembryonic fluid in mice lacking KIF3B motor protein.

Cilia and Hedgehog responsiveness in the mouse.

Author and article information

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