PATTERN & PHENOTYPES
RNA Helicase Mov10 is Essential for Gastrulation
and Central Nervous System Development
Kimberly J. Perry,
Jonathan J. Henry,
* and Stephanie Ceman
Neuroscience Program, University of Illinois-Urbana Champaign, Urbana, Illinois
Cell and Developmental Biology, University of Illinois-Urbana Champaign, Urbana, Illinois
High-Performance Biological Computing, Roy J. Carver Biotechnology Center, University of Illinois-Urbana Champaign, Urbana, Illinois
College of Medicine, University of Illinois-Urbana Champaign, Urbana, Illinois
Background: Mov10 is an RNA helicase that modulates access of Argonaute 2 to microRNA recognition elements in mRNAs.
We examined the role of Mov10 in Xenopus laevis development and show a critical role for Mov10 in gastrulation and in the
development of the central nervous system (CNS).
Results: Knockdown of maternal Mov10 in Xenopus embryos using a trans-
lation blocking morpholino led to defects in gastrulation and the development of notochord and paraxial mesoderm, and a
failure to neurulate. RNA sequencing of the Mov10 knockdown embryos showed signiﬁcant upregulation of many mRNAs
when compared with controls at stage 10.5 (including those related to the cytoskeleton, adhesion, and extracellular matrix,
which are involved in those morphogenetic processes). Additionally, the degradation of the miR-427 target mRNA, cyclin A1,
was delayed in the Mov10 knockdowns. These defects suggest that Mov10’s role in miRNA-mediated regulation of the mater-
nal to zygotic transition could lead to pleiotropic effects that cause the gastrulation defects. Additionally, the knockdown of
zygotic Mov10 showed that it was necessary for normal head, eye, and brain development in Xenopus consistent with a recent
study in the mouse.
Conclusions: Mov10 is essential for gastrulation and normal CNS development. Developmental Dynamics
2017 Wiley Periodicals, Inc.
Key words: RNA helicase; RISC; brain; embryonic development; Mov10; gastrulation
Submitted 9 June 2017; First Decision 21 November 2017; Accepted 18 December 2017; Published online 21 December 2017
The RNA helicase Mov10 was originally described as a cofac-
tor for RNA-induced silencing complex (RISC) component
Argonaute 2 (Ago2) that was required for microRNA (miRNA)-
guided cleavage of a reporter (Meister et al., 2005). Mov10
binds to G-rich secondary structures in mRNAs and unwinds
RNA in a 5
direction in an ATP-dependent manner (Gre-
gersen et al., 2014; Kenny et al., 2014). Mov10 also associates
with nonsense-mediated decay factor UPF1 (Gregersen et al.,
2014). In addition, Mov10 suppresses viral RNAs and retro-
transposition in cultured cells (Burdick et al., 2010; Goodier
et al., 2012). We recently showed that Mov10 is required dur-
ing embryonic development because the Mov10 knockout
mouse is embryonic lethal. As we were unable to identify the
early developmental defects associated with this lethality in
the mouse model (Skariah et al., 2017), we sought to deter-
mine the function of Mov10 in another well-established verte-
brate model system, Xenopus laevis.
Here, we demonstrate a conserved role for Mov10 during
embryonic development in X. laevis. Blocking translation of
maternal Mov10 in X. laevis embryos leads to a severe gastru-
lation defect and failure of the embryo to undergo neurulation.
This may be due to the misregulation of the maternal to zygotic
transition (MZT), where one proposed mechanism involves the
degradation of maternal mRNAs by RISC to permit zygotic
transcription (Tadros and Lipshitz, 2009; Langley et al., 2014).
Loss of zygotic Mov10 using a splice-blocking morpholino in
X. laevis leads to defects in the differentiation of the retina and
abnormalities in brain development. These data agree with our
ﬁndings in mice where, in addition to being essential for early
development, Mov10 expression was found to be signiﬁcantly
elevated in the brain shortly after birth through adolescence
(Skariah et al., 2017). We propose that Mov10 plays a vital role
in gastrulation and normal central nervous system (CNS)
Additional supporting information may be found in the online ver-
sion of this article.
Grant sponsor: National Institute of Mental Health (NIMH) at the
NIH; Grant number: MH093661; Grant sponsor: Spastic Paralysis
Research Foundation of Illinois-Eastern Iowa District of Kiwanis
International; Grant sponsor: National Eye Institute (NEI) at the
NIH; Grant number: EY023979.
†These authors contributed equally to this work.
*Correspondence to: Stephanie Ceman, Neuroscience Program, University
of Illinois-Urbana Champaign, Urbana, IL 61801. E-mail: sceman@illi-
nois.edu or Jonathan J. Henry, Cell and Developmental Biology, Univer-
sity of Illinois-Urbana Champaign, Urbana, Illinois. E-mail: j-henry4@
Article is online at: http://onlinelibrary.wiley.com/doi/10.1002/dvdy.
2017 Wiley Periodicals, Inc.
DEVELOPMENTAL DYNAMICS 247:660–671, 2018