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Developmental biology - Body Symmetry

Origin of Body Asymmetry?

A protein that makes you do the twist...

Asymmetry plays a major role in biology at every scale. Think of DNA spirals, the fact that the human heart is positioned on the left, our preference to use our left or right hand. A team from the Institute of biology Valrose (CNRS/Inserm/Université Côte d'Azur), in collaboration with colleagues from the University of Pennsylvania, has shown how a single protein induces a spiral motion in another molecule.
A single protein induces spiral
motion in another molecule.

Through a domino effect, this causes cells, organs, and indeed the entire body to twist, triggering lateralized behavior. The research is published in the journal Cell: Current Biology on November 23, 2018.
Our world is fundamentally asymmetric. The double helix of DNA, the asymmetric division of stem cells, our human heart positioned on our left. But how do asymmetries emerge, are they linked?

At the Institute of biology Valrose, the team led by the CNRS researcher Stéphane Noselli, which also includes Inserm and Université Cote d'Azur researchers, has been studying right-left asymmetry for several years in order to solve these enigmas. They identified the first gene controlling asymmetry in the common fruit fly (Drosophila), one of the biologists' favored model organisms. More recently, the team showed that this gene plays the same role in vertebrates: the protein that it produces, Myosin 1D, controls the coiling or rotation of organs in the same direction.
The protein Myosin 1D, controls the coiling or rotation of organs in the same direction.

In this new study, researchers induced production of Myosin 1D in the normally symmetrical organs of Drosophila — such as the respiratory trachea. Quite spectacularly, this was enough to induce asymmetry at all levels: deformed cells, trachea coiling around themselves, the twisting of the whole body, and helicoidal locomotive behavior among fly larvae. Remarkably, these new asymmetries always develop in the same direction.

In order to identify the origin of these cascading effects, biochemists from the University of Pennsylvania contributed to the project too: on a glass coverslip, they brought Myosin 1D into contact with a component of cytoskeleton (the cell's "backbone"), namely actin. They were able to observe that the interaction between the two proteins caused the actin to spiral.
Myosin 1D appears to be a unique protein capable of inducing asymmetry in and of itself at all scales, first at the molecular level, then, through a domino effect, at the cell, tissue, and behavioral level.

Besides its role in right-left asymmetry among Drosophila and vertebrates, Myosin 1D appears to be a unique protein that is capable of inducing asymmetry in and of itself at all scales, first at the molecular level, then, through a domino effect, at the cell, tissue, and behavioral level. These results suggest a possible mechanism for the sudden appearance of new morphological characteristics over the course of evolution, such as the twisting of a snail's body.

• The unconventional myosin 1D is required for vertebrate left-right asymmetry
• Loss of myo1d causes aberrant leftward flow and laterality defects in Xenopus
• The function of myosin1D is mediated through the planar cell polarity pathway
Myosin 1D links laterality in arthropods and chordates

Anatomical and functional asymmetries are widespread in the animal kingdom [ 1 , 2 ]. In vertebrates, many visceral organs are asymmetrically placed [ 3 ]. In snails, shells and inner organs coil asymmetrically, and in Drosophila, genitalia and hindgut undergo a chiral rotation during development. The evolutionary origin of these asymmetries remains an open question [ 1 ]. Nodal signaling is widely used [ 4 ], and many, but not all, vertebrates use cilia for symmetry breaking [ 5 ]. In Drosophila, which lacks both cilia and Nodal, the unconventional myosin ID ( myo1d) gene controls dextral rotation of chiral organs [ 6 , 7 ]. Here, we studied the role of myo1d in left-right (LR) axis formation in Xenopus. Morpholino oligomer-mediated myo1d downregulation affected organ placement in >50% of morphant tadpoles. Induction of the left-asymmetric Nodal cascade was aberrant in >70% of cases. Expression of the flow-target gene dand5 was compromised, as was flow itself, due to shorter, fewer, and non-polarized cilia at the LR organizer. Additional phenotypes pinpointed Wnt/planar cell polarity signaling and suggested that myo1d, like in Drosophila [ 8 ], acted in the context of the planar cell polarity pathway. Indeed, convergent extension of gastrula explant cultures was inhibited in myo1d morphants, and the ATF2 reporter gene for non-canonical Wnt signaling was downregulated. Finally, genetic interference experiments demonstrated a functional interaction between the core planar cell polarity signaling gene vangl2 and myo1d in LR axis formation. Thus, our data identified myo1d as a common denominator of arthropod and chordate asymmetry, in agreement with a monophyletic origin of animal asymmetry.

Melanie Tingler, Sabrina Kurz, Markus Maerker, Tim Ott, Franziska Fuhl, Axel Schweickert, Janine M. LeBlanc-Straceski, Stéphane Noselli and Martin Blum.

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Nov 30, 2018   Fetal Timeline   Maternal Timeline   News   News Archive

Myosin 1D alone induces twisting at all scales, affecting the entire organism. Image Credit: CELL.

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