Abstract
BackgroundThe notochord is a signaling center required for the patterning of the vertebrate embryic midline, however, the molecular and cellular mechanisms involved in the formation of this essential embryonic tissue remain unclear. The urochordate Ciona intestinalis develops a simple notochord from 40 specific postmitotic mesodermal cells. The precursors intercalate mediolaterally and establish a single array of disk-shaped notochord cells along the midline. However, the role that notochord precursor polarization, particularly along the dorsoventral axis, plays in this morphogenetic process remains poorly understood.Methodology/Principal FindingsHere we show that the notochord preferentially accumulates an apical cell polarity marker, aPKC, ventrally and a basement membrane marker, laminin, dorsally. This asymmetric accumulation of apicobasal cell polarity markers along the embryonic dorsoventral axis was sustained in notochord precursors during convergence and extension. Further, of several members of the Eph gene family implicated in cellular and tissue morphogenesis, only Ci-Eph4 was predominantly expressed in the notochord throughout cell intercalation. Introduction of a dominant-negative Ci-Eph4 to notochord precursors diminished asymmetric accumulation of apicobasal cell polarity markers, leading to defective intercalation. In contrast, misexpression of a dominant-negative mutant of a planar cell polarity gene Dishevelled preserved asymmetric accumulation of aPKC and laminin in notochord precursors, although their intercalation was incomplete.Conclusions/SignificanceOur data support a model in which in ascidian embryos Eph-dependent dorsoventral polarity of notochord precursors plays a crucial role in mediolateral cell intercalation and is required for proper notochord morphogenesis.
Highlights
Patterning along the midline body axis in vertebrates depends upon signals from a transient embryonic tissue, the notochord [1,2,3]
The specific directional intercalation of notochord plate cells along the mediolateral axis of ciona intestinalis can potentially be explained by several mechanisms, such as a tight intercellular connection [25] and/or a physical barrier that suppresses notochord cell movement along a dorsoventral direction [31,32,33]
To test if the laminin gene is expressed in the notochord plate of Ciona intestinalis embryos, we examined expression of its Ciona intestinalis ortholog Ci-lama3/4/5 by whole mount in situ hybridization
Summary
Patterning along the midline body axis in vertebrates depends upon signals from a transient embryonic tissue, the notochord [1,2,3] This tissue develops from a precursor population that is specified at the posterior midline and elongates anteroposteriorly along the embryonic midline through complex morphogenetic processes during gastrulation and neurulation [4,5,6]. Several molecular components involved in this morphogenetic movement during notochord formation have been identified These include members of the planar cell polarity gene family and the Eph/ephrin gene family [8,9]. The notochord is a signaling center required for the patterning of the vertebrate embryic midline, the molecular and cellular mechanisms involved in the formation of this essential embryonic tissue remain unclear. The role that notochord precursor polarization, along the dorsoventral axis, plays in this morphogenetic process remains poorly understood
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