Atypical Cadherin Dachsous1b Interacts with Ttc28 and Aurora B to Control Microtubule Dynamics in Embryonic Cleavages

Publication date: 7 May 2018
Source:Developmental Cell, Volume 45, Issue 3
Author(s): Jiakun Chen, Gina D. Castelvecchi, Nanbing Li-Villarreal, Brian Raught, Andrzej M. Krezel, Helen McNeill, Lilianna Solnica-Krezel
Atypical cadherin Dachsous (Dchs) is a conserved regulator of planar cell polarity, morphogenesis, and tissue growth during animal development. Dchs functions in part by regulating microtubules by unknown molecular mechanisms. Here we show that maternal zygotic (MZ) dchs1b zebrafish mutants exhibit cleavage furrow progression defects and impaired midzone microtubule assembly associated with decreased microtubule turnover. Mechanistically, Dchs1b interacts via a conserved motif in its intracellular domain with the tetratricopeptide motifs of Ttc28 and regulates its subcellular distribution. Excess Ttc28 impairs cleavages and decreases microtubule turnover, while ttc28 inactivation increases turnover. Moreover, ttc28 deficiency in dchs1b mutants suppresses the microtubule dynamics and midzone microtubule assembly defects. Dchs1b also binds to Aurora B, a known regulator of cleavages and microtubules. Embryonic cleavages in MZdchs1b mutants exhibit increased, and in MZttc28 mutants decreased, sensitivity to Aurora B inhibition. Thus, Dchs1b regulates microtubule dynamics and embryonic cleavages by interacting with Ttc28 and Aurora B.

Teaser

Atypical cadherin Dachsous1b has conserved functions in regulating planar cell polarity and growth in animal development. Chen et al. show that zebrafish Dachsous1b regulates embryonic cleavages and microtubule dynamics through Aurora B and Ttc28. Dachsous1b interacts with Aurora B and Ttc28, via its intracellular domain, and regulates Ttc28 subcellular distribution.


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