Nodal paralogues underlie distinct mechanisms for visceral left–right asymmetry in reptiles and mammals

Kajikawa, Eriko; Horo, Uzuki; Ide, Takahiro; Mizuno, Katsutoshi; Minegishi, Katsura; Hara, Yuichiro; Ikawa, Yayoi; Nishimura, Hiromi; Uchikawa, Masanori; Kanazawa, Hiroshi; Kuraku, Shigehiro; Hamada, Hiroshi

doi:10.1038/s41559-019-1072-2

Cited by 22 publications

(50 citation statements)

References 42 publications

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“…Hereafter, this report will describe L-R symmetry breaking in vertebrates such as mice, frogs, and fish, which is dependent on motile cilia and fluid flow at the LRO (although the description presented is based on studies in mice unless indicated otherwise). Some vertebrates, such as chickens 20 ) and reptiles, 21 ) do not rely on such a mechanism for L-R symmetry breaking. Breaking of L-R symmetry in invertebrates will be described briefly in section 7.…”

Section: Symmetry Breaking At the L-r Organizermentioning

confidence: 99%

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Molecular and cellular basis of left–right asymmetry in vertebrates

Hamada

2020

Proc. Jpn. Acad., Ser. B

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Although the human body appears superficially symmetrical with regard to the left–right (L-R) axis, most visceral organs are asymmetric in terms of their size, shape, or position. Such morphological asymmetries of visceral organs, which are essential for their proper function, are under the control of a genetic pathway that operates in the developing embryo. In many vertebrates including mammals, the breaking of L-R symmetry occurs at a structure known as the L-R organizer (LRO) located at the midline of the developing embryo. This symmetry breaking is followed by transfer of an active form of the signaling molecule Nodal from the LRO to the lateral plate mesoderm (LPM) on the left side, which results in asymmetric expression of Nodal (a left-side determinant) in the left LPM. Finally, L-R asymmetric morphogenesis of visceral organs is induced by Nodal-Pitx2 signaling. This review will describe our current understanding of the mechanisms that underlie the generation of L-R asymmetry in vertebrates, with a focus on mice.

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Section: Symmetry Breaking At the L-r Organizermentioning

confidence: 99%

“…It has also recently been shown that reptile embryos develop L-R asymmetry without motile cilia and fluid flow at the LRO. 21 ) It will thus be of interest to learn the origin of L-R asymmetry in reptiles and birds.…”

Section: Symmetry Breaking At the L-r Organizermentioning

confidence: 99%

Molecular and cellular basis of left–right asymmetry in vertebrates

Hamada

2020

Proc. Jpn. Acad., Ser. B

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“…In vertebrates, two types of LRO have been found: cilia-free LROs, such as Hensen's node in chick, the pig node and the reptilian blastopore; and ciliated LROs, such as the mouse node, the zebrafish Kuppfer's vesicle (KV) and the Xenopus gastrocoel roof plate (Hamada and Tam, 2020;Kajikawa et al, 2020). In chick embryos, leftward movement of Shh + ;Fgf8 + cells around the Hensen's node results in a higher expression level of Nodal in the left side of the node, which then activates Nodal and Pitx2 expression in the left LPM.…”

Section: Nodal Signaling In Left-right Asymmetric Developmentmentioning

confidence: 99%

TGFβ family signaling and development

Jia

Meng

2021

Development

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The transforming growth factor β (TGFβ) signaling family is evolutionarily conserved in metazoans. The signal transduction mechanisms of TGFβ family members have been expansively investigated and are well understood. During development and homeostasis, numerous TGFβ family members are expressed in various cell types with temporally changing levels, playing diverse roles in embryonic development, adult tissue homeostasis and human diseases by regulating cell proliferation, differentiation, adhesion, migration and apoptosis. Here, we discuss the molecular mechanisms underlying signal transduction and regulation of the TGFβ subfamily pathways, and then highlight their key functions in mesendoderm induction, dorsoventral patterning and laterality development, as well as in the formation of several representative tissues/organs.

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“…Nodal then activates expression of the transcription factor Pitx2 in the left LPM and, ultimately, on the left side of developing organs, where it is required for the proper morphogenesis of various anatomical asymmetries (Burn and Hill, 2009;Campione et al, 1999;Davis et al, 2017;Liu et al, 2001;Mahadevan et al, 2014;Muller et al, 2003;Plageman et al, 2011;Ryan et al, 1998;Welsh et al, 2013;Womble et al, 2018). In some species, cilia are not involved and the early symmetry-breaking events remain unclear (Gros et al, 2009;Hamada and Tam, 2020;Kajikawa et al, 2020); nonetheless, the process culminates in LR asymmetrical gene expression in the LPM.…”

Section: Introductionmentioning

confidence: 99%

The twists and turns of left-right asymmetric gut morphogenesis

2020

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Many organs develop left-right asymmetric shapes and positions that are crucial for normal function. Indeed, anomalous laterality is associated with multiple severe birth defects. Although the events that initially orient the left-right body axis are beginning to be understood, the mechanisms that shape the asymmetries of individual organs remain less clear. Here, we summarize new evidence challenging century-old ideas about the development of stomach and intestine laterality. We compare classical and contemporary models of asymmetric gut morphogenesis and highlight key unanswered questions for future investigation.

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Nodal paralogues underlie distinct mechanisms for visceral left–right asymmetry in reptiles and mammals

Cited by 22 publications

References 42 publications

Molecular and cellular basis of left–right asymmetry in vertebrates

Molecular and cellular basis of left–right asymmetry in vertebrates

TGFβ family signaling and development

The twists and turns of left-right asymmetric gut morphogenesis

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