The intracellular interactions of the L1 family of cell adhesion molecules

Herron, Lissa R.; Hill, Maria; Davey, Fleur; Gunn‐Moore, Frank

doi:10.1042/bj20082284

Cited by 56 publications

(42 citation statements)

References 132 publications

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“…NrCAM is known to interact with a number of intracellular binding partners, including: FERMdomain proteins; the PDZ-containing proteins SAP102 and SAP97; members of the membrane-associated guanylate kinases (MAGUK) family; and GIPC proteins (Herron et al, 2009). SAP102 is expressed in GNs and a form of NrCAM lacking the Cterminal PDZ-binding motif suppressed GN neurite outgrowth (Davey et al, 2005); however, effects on proliferation were not assessed.…”

Section: Nrcam Is Required For Anti-proliferative Effects Of F3mentioning

confidence: 99%

“…A further candidate for modulating GNP cell cycle exit is the immunoglobulin-like adhesion molecule F3/contactin (F3), one of six glycosyl phosphatidyl inositol (GPI)-linked contactins (CNTNs) that, together with their cognate and related partners, the L1-like proteins (Brummendorf and Rathjen, 1996), form the L1-CNTN family of cell-adhesion molecules (Herron et al, 2009;Katidou et al, 2008). Like vitronectin, F3 is strongly expressed on postmitotic GNs and their axons (Faivre-Sarrailh et al, 1992;Virgintino et al, 1999;Yoshihara et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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F3/contactin and TAG1 play antagonistic roles in the regulation of sonic hedgehog-induced cerebellar granule neuron progenitor proliferation

et al. 2011

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SUMMARYModulation of the sonic hedgehog (SHH) pathway is a crucial factor in cerebellar morphogenesis. Stimulation of granule neuron progenitor (GNP) proliferation is a central function of SHH signalling, but how this is controlled locally is not understood. We show that two sequentially expressed members of the contactin (CNTN) family of adhesion molecules, TAG1 and F3, act antagonistically to control SHH-induced proliferation: F3 suppresses SHH-induced GNP proliferation and induces differentiation, whereas TAG1 antagonises F3. Production of GNPs in TAG1-null mice is delayed and reduced. F3 and TAG1 colocalise on GNPs with the related L1-like adhesion molecule NrCAM, and F3 fails to suppress the SHH-induced proliferation of NrCAM-deficient GNPs. We show that F3 and SHH both primarily affect a group of intermediate GNPs (IPs), which, though actively dividing, also express molecules associated with differentiation, including -tubulin III (TuJ1) and TAG1. In vivo, intermediate progenitors form a discrete layer in the middle of the external germinal layer (mEGL), while F3 becomes expressed on the axons of postmitotic granule neurons as they leave the inner EGL (iEGL). We propose, therefore, that F3 acts as a localised signal in the iEGL that induces SHH-stimulated cells in the overlying mEGL to exit cell cycle and differentiate. By contrast, expression of TAG1 on GNPs antagonises this signal in the mEGL, preventing premature differentiation and sustaining GNP expansion in a paracrine fashion. Together, these findings indicate that CNTN and L1-like proteins play a significant role in modulating SHH-induced neuronal precursor proliferation.

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Section: Nrcam Is Required For Anti-proliferative Effects Of F3mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

F3/contactin and TAG1 play antagonistic roles in the regulation of sonic hedgehog-induced cerebellar granule neuron progenitor proliferation

et al. 2011

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“…Nevertheless, these alterations seem to be relevant also in pancreatic tumorigenesis and we will therefore discuss findings on the role of L1CAM in tumor manifestation and progression from studies with PDAC as well as other tumor entities. We also like to refer to the excellent reviews outlining in more detail the current knowledge on L1CAM-mediated signalling (Herron et al, 2009;Kiefel et al, 2011).…”

Section: L1cam Function In Tumorigenesismentioning

confidence: 99%

The Adhesion Molecule L1CAM as a Novel Therapeutic Target for Treatment of Pancreatic Cancer Patients?

Sebens¹,

Schäfer²

2012

Pancreatic Cancer - Molecular Mechanism and Targets

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“…Conventional -spectrins are well known to associate with IgCAMs of the L1 subfamily via the adapter molecule Ankyrin (Herron et al, 2009;Hortsch et al, 2009). Roughest belongs to a different subfamily that includes Nephrin and has a completely divergent cytoplasmic domain that lacks the conventional Ankryin binding site (Strunkelnberg et al, 2003).…”

Section: Spectrin and Ig-camsmentioning

confidence: 99%

“…Roughest is a member of the immunoglobulin superfamily of cell adhesion molecules (Ig-CAM). The L1 subset of this superfamily interacts with conventional -spectrin via the adaptor protein Ankyrin (Herron et al, 2009;Hortsch et al, 2009). However, neither Roughest nor  H contains a recognizable Ankyrin binding site (Strunkelnberg et al, 2003;Thomas et al, 1997).…”

mentioning

confidence: 99%

The cell adhesion molecule Roughest depends on βHeavy-spectrin during eye morphogenesis in Drosophila

Lee

Zarnescu

MacIver

et al. 2010

Journal of Cell Science

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SummaryCell junctions have both structural and morphogenetic roles, and contain complex mixtures of proteins whose interdependencies are still largely unknown. Junctions are also major signaling centers that signify correct integration into a tissue, and modulate cell survival. During Drosophila eye development, the activity of the immunoglobulin cell adhesion molecule Roughest (also known as Irregular chiasm C-roughest protein) mediates interommatidial cell (IOC) reorganization, leading to an apoptotic event that refines the retinal lattice. Roughest and the cadherin-based zonula adherens (ZA) are interdependent and both are modulated by the apical polarity determinant, Crumbs. Here we describe a novel relationship between the Crumbs partner  Heavy -spectrin ( H ), the ZA and Roughest. Ectopic expression of the C-terminal segment 33 of  H (H33) induces defects in retinal morphogenesis, resulting the preferential loss of IOC. This effect is associated with ZA disruption and Roughest displacement. In addition, loss-of-function karst and roughest mutations interact to cause a synergistic and catastrophic effect on retinal development. Finally, we show that  H coimmunoprecipitates with Roughest and that the distribution of Roughest protein is disrupted in karst mutant tissue. These results suggest that the apical spectrin membrane skeleton helps to coordinate the Cadherin-based ZA with Roughest-based morphogenesis.Key words: Drosophila, Cell adhesion, Apoptosis, Spectrin, Membrane skeleton, Crumbs, IrreC, Roughest Journal of Cell Science 278Phillips and Thomas, 2006;Stabach et al., 2009) activities, spectrins can variously stabilize proteins at the membrane, nucleate protein complexes and modulate protein delivery and recycling. The Crumbs- H complex has been implicated in the development and maintenance of the apical domain via the modulation of endocytosis in both lossof-function and gain-of-function experiments (Pellikka et al., 2002;Williams et al., 2004). This activity appears to be centered on the Cterminal segment 33 of  H (H33), the overexpression of which causes membrane growth and the sequestration of Dynamin (Williams et al., 2004). In some tissues, expression of H33 also induces apoptosis (Williams et al., 2004). These phenotypes are  H specific, because overexpression of the equivalent region of the basolateral -spectrin does not have this effect (Williams et al., 2004). Modulation of endocytosis or recycling of junctional proteins through interactions with segment 33 of  H might thus provide the normal mechanism whereby the ZA is stabilized.Here, we further characterize the effects of H33 in the developing eye. We find that H33 expression preferentially results in the loss of IOC. We further show that these defects in morphogenesis are associated with fragmentation of the ZA and disruption of the Ig-CAM Roughest. In addition, we show that  H genetically and physically interacts with Roughest to maintain its wild-type distribution. Because  H also supports the ZA, we suggest that the ac...

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The intracellular interactions of the L1 family of cell adhesion molecules

Cited by 56 publications

References 132 publications

F3/contactin and TAG1 play antagonistic roles in the regulation of sonic hedgehog-induced cerebellar granule neuron progenitor proliferation

F3/contactin and TAG1 play antagonistic roles in the regulation of sonic hedgehog-induced cerebellar granule neuron progenitor proliferation

The Adhesion Molecule L1CAM as a Novel Therapeutic Target for Treatment of Pancreatic Cancer Patients?

The cell adhesion molecule Roughest depends on βHeavy-spectrin during eye morphogenesis in Drosophila

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