Cytokinetic bridge triggers de novo lumen formation in vivo

L. I. Rathbun, E. G. Colicino, J. Manikas, J. O’Connell, N. Krishnan, N. S. Reilly, S. Coyne, G. Erdemci-Tandogan, A. Garrastegui, J. Freshour, P. Santra, M. L. Manning, J. D. Amack and H. Hehnly ()
Additional contact information
L. I. Rathbun: Syracuse University
E. G. Colicino: Syracuse University
J. Manikas: Syracuse University
J. O’Connell: Syracuse University
N. Krishnan: Syracuse University
N. S. Reilly: University of Rochester
S. Coyne: SUNY Upstate Medical School
G. Erdemci-Tandogan: Syracuse University
A. Garrastegui: Syracuse University
J. Freshour: Syracuse University
P. Santra: SUNY Upstate Medical School
M. L. Manning: Syracuse University
J. D. Amack: SUNY Upstate Medical School
H. Hehnly: Syracuse University

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract Multicellular rosettes are transient epithelial structures that serve as intermediates during diverse organ formation. We have identified a unique contributor to rosette formation in zebrafish Kupffer’s vesicle (KV) that requires cell division, specifically the final stage of mitosis termed abscission. KV utilizes a rosette as a prerequisite before forming a lumen surrounded by ciliated epithelial cells. Our studies identify that KV-destined cells remain interconnected by cytokinetic bridges that position at the rosette’s center. These bridges act as a landmark for directed Rab11 vesicle motility to deliver an essential cargo for lumen formation, CFTR (cystic fibrosis transmembrane conductance regulator). Here we report that premature bridge cleavage through laser ablation or inhibiting abscission using optogenetic clustering of Rab11 result in disrupted lumen formation. We present a model in which KV mitotic cells strategically place their cytokinetic bridges at the rosette center, where Rab11-associated vesicles transport CFTR to aid in lumen establishment.

Date: 2020
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DOI: 10.1038/s41467-020-15002-8

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