Data from: Formin is associated with left-right asymmetry in the pond snail and the frog
Data files
Jan 19, 2017 version files 246.98 MB
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BAC_assembly.fasta.gz
292.02 KB
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Euhadra_formin_intron_sequence.fas
80.33 KB
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FH2_animals.fas
26.72 KB
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gastropods_fh2_domain_aligned.fas
37.96 KB
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gLs.scaffolds.fa.gz
246.28 MB
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Ldia_aligned.fas
34.91 KB
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Lfry_Ltud_Lprcp_Lmfsd.fas
31.08 KB
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LSU_SSU.fas
129.90 KB
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Partula_formin_intron_sequences.fas
20.83 KB
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qPCR_raw_data_relates_to_Fig1_FigS2a.xlsx
18.50 KB
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Table S1.xlsx
29.93 KB
Abstract
While components of the pathway that establishes left-right asymmetry have been identified in diverse animals, from vertebrates to flies, it is striking that the genes involved in the first symmetry-breaking step remain wholly unknown in the most obviously chiral animals, the gastropod snails. Previously, research on snails was used to show that left-right signaling of Nodal, downstream of symmetry breaking, may be an ancestral feature of the Bilateria. Here, we report that a disabling mutation in one copy of a tandemly duplicated, diaphanous-related formin is perfectly associated with symmetry breaking in the pond snail. This is supported by the observation that an anti-formin drug treatment converts dextral snail embryos to a sinistral phenocopy, and in frogs, drug inhibition or overexpression by microinjection of formin has a chirality-randomizing effect in early (pre-cilia) embryos. Contrary to expectations based on existing models, we discovered asymmetric gene expression in 2- and 4-cell snail embryos, preceding morphological asymmetry. As the formin-actin filament has been shown to be part of an asymmetry-breaking switch in vitro, together these results are consistent with the view that animals with diverse body plans may derive their asymmetries from the same intracellular chiral elements.