scholarly journals Myosin1D is an evolutionarily conserved determinant of animal Left/Right asymmetry

2018 ◽  
Author(s):  
Thomas Juan ◽  
Charles Géminard ◽  
Jean-Baptiste Coutelis ◽  
Delphine Cerezo ◽  
Sophie Polès ◽  
...  

The establishment of Left/Right (LR) asymmetry is fundamental to animal development. While the pathways governing antero-posterior and dorso-ventral patterning are well conserved among different phyla, divergent mechanisms have been implicated in the specification of LR asymmetry in vertebrates and invertebrates. A cilia-driven, directional fluid flow is important for symmetry breaking in numerous vertebrates, including zebrafish1–10. Alternatively, LR asymmetry can be established independently of motile cilia, notably through the intrinsic chirality of the acto-myosin cytoskeleton11–18. Here we show that MyosiniD (Myo1D), which has been previously identified as a key determinant of LR asymmetry in Drosophila12,13, is essential for the formation and the function of the zebrafish LR Organizer (LRO). We show that Myo1D controls the polarity of LRO cilia and interacts functionally with the Planar Cell Polarity (PCP) gene VanGogh-like2 (Vangl2)19, to promote the establishment of a functional LRO flow. Our findings identify Myo1D as the first evolutionarily conserved determinant of LR asymmetry, and show that functional interactions between Myo1D and PCP are central to the establishment of animal LR asymmetry.

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 123 ◽  
Author(s):  
Hiroshi Hamada ◽  
Patrick Tam

Left-right (L-R) asymmetry of visceral organs in animals is established during embryonic development via a stepwise process. While some steps are conserved, different strategies are employed among animals for initiating the breaking of body symmetry. In zebrafish (teleost), Xenopus (amphibian), and mice (mammal), symmetry breaking is elicited by directional fluid flow at the L-R organizer, which is generated by motile cilia and sensed by mechanoresponsive cells. In contrast, birds and reptiles do not rely on the cilia-driven fluid flow. Invertebrates such as Drosophila and snails employ another distinct mechanism, where the symmetry breaking process is underpinned by cellular chirality acquired downstream of the molecular interaction of myosin and actin. Here, we highlight the convergent entry point of actomyosin interaction and planar cell polarity to the diverse L-R symmetry breaking mechanisms among animals.


2010 ◽  
Vol 12 (5) ◽  
pp. 520-520 ◽  
Author(s):  
Boris Guirao ◽  
Alice Meunier ◽  
Stéphane Mortaud ◽  
Andrea Aguilar ◽  
Jean-Marc Corsi ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0153144 ◽  
Author(s):  
Anny Caceres Treat ◽  
David S. Wheeler ◽  
Donna B. Stolz ◽  
Michael Tsang ◽  
Peter A. Friedman ◽  
...  

2016 ◽  
Vol 113 (50) ◽  
pp. E8079-E8088 ◽  
Author(s):  
Jia Yuan ◽  
Jeeyeon Cha ◽  
Wenbo Deng ◽  
Amanda Bartos ◽  
Xiaofei Sun ◽  
...  

Blastocyst implantation is a complex process requiring coordination of a dynamic sequence of embryo–uterine interactions. Blood vessels enter the uterus from the mesometrium, demarcating the uterus into mesometrial (M) and antimesometrial (AM) domains. Implantation occurs along the uterine longitudinal axis within specialized implantation chambers (crypts) that originate within the evaginations directed from the primary lumen toward the AM domain. The morphological orientation of crypts in rodent uteri was recognized more than a century ago, but the mechanism remained unknown. Here we provide evidence that planar cell polarity (PCP) signaling orchestrates directed epithelial evaginations to form crypts for implantation in mice. Uterine deletion of Vang-like protein 2, but not Vang-like protein 1, conferred aberrant PCP signaling, misdirected epithelial evaginations, defective crypt formation, and blastocyst attachment, leading to severely compromised pregnancy outcomes. The study reveals a previously unrecognized role for PCP in executing spatial cues for crypt formation and implantation. Because PCP is an evolutionarily conserved phenomenon, our study is likely to inspire implantation studies of this signaling pathway in humans and other species.


2014 ◽  
Vol 25 (8) ◽  
pp. 1276-1286 ◽  
Author(s):  
Fabien Soulavie ◽  
David Piepenbrock ◽  
Joëlle Thomas ◽  
Jennifer Vieillard ◽  
Jean-Luc Duteyrat ◽  
...  

Cilia play major functions in physiology and development, and ciliary dysfunctions are responsible for several diseases in humans called ciliopathies. Cilia motility is required for cell and fluid propulsion in organisms. In humans, cilia motility deficiencies lead to primary ciliary dyskinesia, with upper-airways recurrent infections, left–right asymmetry perturbations, and fertility defects. In Drosophila, we identified hemingway (hmw) as a novel component required for motile cilia function. hmw encodes a 604–amino acid protein characterized by a highly conserved coiled-coil domain also found in the human orthologue, KIAA1430. We show that HMW is conserved in species with motile cilia and that, in Drosophila, hmw is expressed in ciliated sensory neurons and spermatozoa. We created hmw-knockout flies and found that they are hearing impaired and male sterile. hmw is implicated in the motility of ciliated auditory sensory neurons and, in the testis, is required for elongation and maintenance of sperm flagella. Because HMW is absent from mature flagella, we propose that HMW is not a structural component of the motile axoneme but is required for proper acquisition of motile properties. This identifies HMW as a novel, evolutionarily conserved component necessary for motile cilium function and flagella assembly.


Development ◽  
2020 ◽  
Vol 147 (19) ◽  
pp. dev191981 ◽  
Author(s):  
Elvis Huarcaya Najarro ◽  
Jennifer Huang ◽  
Adrian Jacobo ◽  
Lee A. Quiruz ◽  
Nicolas Grillet ◽  
...  

ABSTRACTPlanar cell polarity (PCP) proteins localize asymmetrically to instruct cell polarity within the tissue plane, with defects leading to deformities of the limbs, neural tube and inner ear. Wnt proteins are evolutionarily conserved polarity cues, yet Wnt mutants display variable PCP defects; thus, how Wnts regulate PCP remains unresolved. Here, we have used the developing cochlea as a model system to show that secreted Wnts regulate PCP through polarizing a specific subset of PCP proteins. Conditional deletion of Wntless or porcupine, both of which are essential for secretion of Wnts, caused misrotated sensory cells and shortened cochlea – both hallmarks of PCP defects. Wntless-deficient cochleae lacked the polarized PCP components dishevelled 1/2 and frizzled 3/6, while other PCP proteins (Vangl1/2, Celsr1 and dishevelled 3) remained localized. We identified seven Wnt paralogues, including the major PCP regulator Wnt5a, which was, surprisingly, dispensable for planar polarization in the cochlea. Finally, Vangl2 haploinsufficiency markedly accentuated sensory cell polarization defects in Wntless-deficient cochlea. Together, our study indicates that secreted Wnts and Vangl2 coordinate to ensure proper tissue polarization during development.


2018 ◽  
Author(s):  
Hanh Thi-Kim Vu ◽  
Sarah Mansour ◽  
Michael Kücken ◽  
Corinna Blasse ◽  
Cyril Basquin ◽  
...  

SummaryPolarity is a universal design principle of biological systems that manifests at all organizational scales. Although well understood at the cellular level, the mechanisms that coordinate polarity at the tissue or organismal scale remain poorly understood. Here, we make use of the extreme body plan plasticity of planarian flatworms to probe the multi-scale coordination of polarity. Quantitative analysis of ciliary rootlet orientation in the epidermis reveals a global polarization field with head and tail as independent mediators of anteroposterior (A/P) polarization and the body margin influencing mediolateral (M/L) polarization. Mathematical modeling demonstrates that superposition of separate A/P- and M/L-fields can explain the global polarity field and we identify the core planar cell polarity (PCP) and Ft/Ds pathways as their specific mediators. Overall, our study establishes a mechanistic framework for the multi-scale coordination of planar polarity in planarians and establishes the core PCP and Ft/Ds pathways as evolutionarily conserved 2D-polarization module.


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