Identification of a novel left–right asymmetrically expressed gene in the mouse belonging to the BPI/PLUNC superfamily

Hou, Juan; Yashiro, Kenta; Okazaki, Yasushi; Saijoh, Yukio; Hayashizaki, Yoshihide; Hamada, Hiroshi

doi:10.1002/dvdy.10450

Cited by 18 publications

(21 citation statements)

References 40 publications

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“…LPlunc1 was expressed normally in crown cells of the node with the normal strong leftward bias at 7 sp (n = 4) ( Fig. 3I,J ;Hou et al 2004). Collectively, these results suggest that the node is properly formed and patterned in the absence of Smad1.…”

Section: Node and Midline Markers Are Not Affected In Smad1-null Embryosmentioning

confidence: 66%

BMP/SMAD1 signaling sets a threshold for the left/right pathway in lateral plate mesoderm and limits availability of SMAD4

Furtado¹,

Solloway²,

Jones³

et al. 2008

Genes Dev.

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The left/right (LR) axial pathway establishes asymmetry in the patterning and morphogenesis of multiple internal organs, including the heart. In mammals, this pathway involves the breaking of molecular symmetry in or around the node, transfer of asymmetry information to the lateral plate mesoderm (LPM), propagation of molecular asymmetries throughout the LPM, and interpretation of these signals for proper organ morphogenesis (Nonaka et al. 2002). Recent experiments have demonstrated that the breaking of bilateral symmetry in the mouse node occurs via a process termed "nodal flow," in which motile cilia in the node generate leftward movement of molecular determinants via lipoprotein vesicles (Hirokawa et al. 2006;. NODAL, a transforming growth factor ␤ (TGF␤) superfamily member, is a key molecule in the LR cascade. NODAL acts first in mesoderm specification and anterior-posterior axis formation, signaling through a membrane complex containing type I and II TGF␤ serine/ threonine kinase receptors, as well as GPI-anchored members of the EGF-CFC family. This complex phosphorylates intracellular SMAD2 and SMAD3, which associate with the common TGF␤/NODAL/BMP (bone morphogenetic protein) pathway SMAD, SMAD4, and forkhead transcription factor FOXH1, to regulate downstream target genes (Shen 2007). In the LR pathway,

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Section: Node and Midline Markers Are Not Affected In Smad1-null Embryosmentioning

confidence: 66%

BMP/SMAD1 signaling sets a threshold for the left/right pathway in lateral plate mesoderm and limits availability of SMAD4

Furtado¹,

Solloway²,

Jones³

et al. 2008

Genes Dev.

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“…The size of the SPLUNC1 protein is about 24 kDa adipose cells , which indicated that the SPLUNC1 expression has the specificity of development stage and species. Another member of PLUNC family, LPLUNC1, was also found to be periodical expressed during the development of the mouse, its expression is first detected at embryonic day 7.5 and disappears at the eight to ten somite stage of development (Hou et al 2004). Its location at the absorptive cell may also contribute to the lipid absorption of intestine.…”

Section: Resultsmentioning

confidence: 97%

Tissue distribution of the secretory protein, SPLUNC1, in the human fetus

Zhou

Fan

Zhao

et al. 2005

Histochem Cell Biol

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We previously identified a tissue-specific gene, short palate, lung, and nasal epithelium clone 1 (SPLUNC1), in nasopharyngeal epithelial tissues. SPLUNC1 was differentially expressed in nasopharyngeal carcinoma. Bioinformatic analysis revealed that SPLUNC1 has the bactericidal permeability-increasing protein/lipid-binding protein (BPI/LBP) domain and a 19 amino acid signal peptide, which suggest that it is a secretory protein. Its precise cellular localization in the respiratory tract is mainly in mucous cells and ducts of submucosal glands. However, little is known about its expression pattern in various human tissues. We generated a highly specific antibody and analyzed its distribution in the human fetus by immunohistochemistry to more precisely determine SPLUNC1 protein localization in human tissues. The results were further validated by RT-PCR. Our results showed that SPLUNC1 protein is expressed at not only the serous glands and epithelium of the upper respiratory tract and digestive tract, but also in the oculi of human embryos. Interestingly, we also found positive staining in fetus adipose tissue, a result not previously reported in studies of adult human tissues. Western blot analysis detected a 24 kDa SPLUNC1 protein in the compounds of nasopharyngeal secretions. This secretory protein was also detected in saliva and tears. Our research suggests that SPLUNC1 protein may not only be an antimicrobial peptide that plays an important role in the maintenance of homeostasis in the upper respiratory tract, oculi, and alimentary tract, it may also be important in the development and lipid metabolism of the adipose tissue.

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“…Therefore, other genes expressed in the node with subtle asymmetry, such as LPlunc1 and Cerberus-like 2, may play a role in this process (Hou et al, 2004;Marques et al, 2004;Pearce et al, 1999).…”

Section: How Does Bilateral Nodal Expression In the Node Results In Asmentioning

confidence: 99%

Sulfated glycosaminoglycans are necessary for Nodal signal transmission from the node to the left lateral plate in the mouse embryo

Hashimoto²,

et al. 2007

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Situs-specific organogenesis in the mouse results from leftward fluid flow in the node cavity and subsequent left-sided expression of Nodal in the lateral plate mesoderm (LPM). Nodal expression at the node is essential for the subsequent asymmetric Nodal expression in the left LPM, but the precise role of Nodal produced at the node has remained unknown. We have now investigated how the Nodal signal is transferred from the node to the LPM. Externally supplied Nodal protein failed to signal to the LPM,suggesting that the Nodal signal is transferred to the LPM via an internal route rather than an external one. Transgenic rescue experiments showed that the Nodal co-receptor Cryptic (Cfc1) is required only in the LPM, not at the node, for asymmetric Nodal expression in the LPM, indicating that the Nodal signal is not relayed indirectly between the node and LPM. Nodal interacts in vitro with sulfated glycosaminoglycans (GAGs), which are specifically localized to the basement membrane-like structure between the node and LPM in the mouse embryo. Inhibition of sulfated GAG biosynthesis prevents Nodal expression in the LPM. These data suggest that Nodal produced at the node might travel directly to the LPM via interaction with sulfated GAGs.

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Identification of a novel left–right asymmetrically expressed gene in the mouse belonging to the BPI/PLUNC superfamily

Cited by 18 publications

References 40 publications

BMP/SMAD1 signaling sets a threshold for the left/right pathway in lateral plate mesoderm and limits availability of SMAD4

BMP/SMAD1 signaling sets a threshold for the left/right pathway in lateral plate mesoderm and limits availability of SMAD4

Tissue distribution of the secretory protein, SPLUNC1, in the human fetus

Sulfated glycosaminoglycans are necessary for Nodal signal transmission from the node to the left lateral plate in the mouse embryo

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