Low Frequency Vibrations Disrupt Left-Right Patterning in the Xenopus Embryo

The development of consistent left-right (LR) asymmetry across phyla is a fascinating question in biology. While many pharmacological and molecular approaches have been used to explore molecular mechanisms, it has proven difficult to exert precise temporal control over functional perturbations. Here, we took advantage of acoustical vibration to disrupt LR patterning in Xenopus embryos during tightly-circumscribed periods of development. Exposure to several low frequencies induced specific randomization of three internal organs (heterotaxia). Investigating one frequency (7 Hz), we found two discrete periods of sensitivity to vibration; during the first period, vibration affected the same LR pathway as nocodazole, while during the second period, vibration affected the integrity of the epithelial barrier; both are required for normal LR patterning. Our results indicate that low frequency vibrations disrupt two steps in the early LR pathway: the orientation of the LR axis with the other two axes, and the amplification/restriction of downstream LR signals to asymmetric organs

Rab6 and myosin II at the cutting edge of membrane fission

Rab GTPases regulate the dynamics of transport carriers by participating in their translocation across the cytoplasm, and in their docking and fusion with acceptor compartments. An interaction between Golgi-associated Rab6 and myosin II has now been shown to regulate the fission of Rab6-positive carriers, illuminating a previously unappreciated role for Rab6 and the actomyosin system in carrier biogenesis

Epistasis regulates the developmental stability of the mouse craniofacial shape.

12 pagesInternational audienceFluctuating asymmetry is a classic concept linked to organismal development. It has traditionally been used as a measure ofdevelopmental instability, which is the inability of an organism to buffer environmental fluctuations during development.Developmental stability has a genetic component that influences the final phenotype of the organism and can lead tocongenital disorders. According to alternative hypotheses, this genetic component might be either the result of additivegenetic effects or a by-product of developmental gene networks. Here we present a genome-wide association study of thegenetic architecture of fluctuating asymmetry of the skull shape in mice. Geometric morphometric methods were applied toquantify fluctuating asymmetry: we estimated fluctuating asymmetry as Mahalanobis distances to the mean asymmetry,correcting first for genetic directional asymmetry. We applied the marginal epistasis test to study epistasis among genomicregions. Results showed no evidence of additive effects but several interacting regions significantly associated withfluctuating asymmetry. Among the candidate genes overlapping these interacting regions we found an over-representation ofgenes involved in craniofacial development. A gene network is likely to be associated with skull developmental stability, andgenes originally described as buffering genes (e.g., Hspa2) might occupy central positions within these networks, whereregulatory elements may also play an important role. Our results constitute an important step in the exploration of themolecular roots of developmental stability and the first empirical evidence about its genetic architecture