RT Journal Article
SR Electronic
T1 Myosin1G promotes Nodal signaling to control Zebrafish Left-Right asymmetry
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2023.09.15.557992
DO 10.1101/2023.09.15.557992
A1 Kurup, Akshai Janardhana
A1 Bailet, Florian
A1 Fürthauer, Maximilian
YR 2023
UL http://biorxiv.org/content/early/2023/09/15/2023.09.15.557992.abstract
AB Myosin1D (Myo1D) has recently emerged as a conserved regulator of animal LR asymmetry that governs the morphogenesis of the central LR Organizer (LRO). In addition to Myo1D, the zebrafish genome encodes the closely related Myo1G. While Myo1G also controls LR asymmetry, we show that it does so through an entirely different mechanism. Myo1G promotes the Nodal-mediated transfer of laterality information from the LRO to target tissues. At the cellular level, Myo1G is associated with endosomes positive for the TGFβ signaling adapter SARA. myo1g mutants have fewer SARA-positive Activin receptor endosomes and a reduced responsiveness to Nodal ligands that results in a delay of left-sided Nodal propagation and tissue-specific laterality defects in organs that are most distant from the LRO. Beyond LR asymmetry, Myo1G promotes signaling by different Nodal ligands in other biological contexts. Our findings therefore identify Myo1G as a novel positive regulator of the Nodal signaling pathway.Competing Interest StatementThe authors have declared no competing interest.