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The single Drosophila ZO-1 protein Polychaetoid regulates embryonic morphogenesis in coordination with Canoe/afadin and Enabled.

Choi W, Jung KC, Nelson KS, Bhat MA, Beitel GJ, Peifer M, Fanning AS - Mol. Biol. Cell (2011)

Bottom Line: Pyd loss does not dramatically affect AJ protein localization or initial localization of actin and myosin during dorsal closure.The defects, which include segmental grooves that fail to retract, a disrupted leading edge actin cable, and reduced zippering as leading edges meet, closely resemble defects in canoe zygotic mutants and in embryos lacking the actin regulator Enabled (Ena), suggesting that these proteins act together.Canoe (Cno) and Pyd are required for proper Ena localization during dorsal closure, and strong genetic interactions suggest that Cno, Pyd, and Ena act together in regulating or anchoring the actin cytoskeleton during dorsal closure.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of North Carolina at Chapel Hill, USA.

ABSTRACT
Adherens and tight junctions play key roles in assembling epithelia and maintaining barriers. In cell culture zonula occludens (ZO)-family proteins are important for assembly/maturation of both tight and adherens junctions (AJs). Genetic studies suggest that ZO proteins are important during normal development, but interpretation of mouse and fly studies is limited by genetic redundancy and/or a lack of alleles. We generated alleles of the single Drosophila ZO protein Polychaetoid (Pyd). Most embryos lacking Pyd die with striking defects in morphogenesis of embryonic epithelia including the epidermis, segmental grooves, and tracheal system. Pyd loss does not dramatically affect AJ protein localization or initial localization of actin and myosin during dorsal closure. However, Pyd loss does affect several cell behaviors that drive dorsal closure. The defects, which include segmental grooves that fail to retract, a disrupted leading edge actin cable, and reduced zippering as leading edges meet, closely resemble defects in canoe zygotic mutants and in embryos lacking the actin regulator Enabled (Ena), suggesting that these proteins act together. Canoe (Cno) and Pyd are required for proper Ena localization during dorsal closure, and strong genetic interactions suggest that Cno, Pyd, and Ena act together in regulating or anchoring the actin cytoskeleton during dorsal closure.

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pydMZ mutants have defects in head involution but do not have serious deficits in Notch signaling. (A–C) Cuticles of pydMZ mutant embryos. (A) Example of wild-type phenotype, with intact head skeleton (arrow). (B) Example of defects in the head skeleton, indicative of defects in head involution. (C) Example of complete failure of head involution. (D) Percentages of dead embryos in each phenotypic class for different allelic combinations of pyd alleles. (E–G) Central nervous system revealed by phalloidin staining for actin. pydMZ mutants do not exhibit obvious nervous system hypertrophy, although some had modest defects in axon architecture (G). Scale bars, 75 μm.
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Figure 2: pydMZ mutants have defects in head involution but do not have serious deficits in Notch signaling. (A–C) Cuticles of pydMZ mutant embryos. (A) Example of wild-type phenotype, with intact head skeleton (arrow). (B) Example of defects in the head skeleton, indicative of defects in head involution. (C) Example of complete failure of head involution. (D) Percentages of dead embryos in each phenotypic class for different allelic combinations of pyd alleles. (E–G) Central nervous system revealed by phalloidin staining for actin. pydMZ mutants do not exhibit obvious nervous system hypertrophy, although some had modest defects in axon architecture (G). Scale bars, 75 μm.

Mentions: As a first assessment of the embryonic processes affected by Pyd loss, we examined the cuticles of mutant embryos at the end of embryogenesis. The cuticle is secreted by epidermal cells and provides a clear readout of cell fate choices and successful completion of morphogenetic movements. In wild-type embryos, cells of the head segments move forward and inward in a process called head involution and then secrete the specialized cuticle of the mouth parts (Figure 2A, arrow). At roughly the same time, lateral sheets of cells of the thoracic and abdominal epidermis move toward the dorsal midline, meeting and zipping closed in a process known as dorsal closure, resulting in an intact dorsal cuticle.


The single Drosophila ZO-1 protein Polychaetoid regulates embryonic morphogenesis in coordination with Canoe/afadin and Enabled.

Choi W, Jung KC, Nelson KS, Bhat MA, Beitel GJ, Peifer M, Fanning AS - Mol. Biol. Cell (2011)

pydMZ mutants have defects in head involution but do not have serious deficits in Notch signaling. (A–C) Cuticles of pydMZ mutant embryos. (A) Example of wild-type phenotype, with intact head skeleton (arrow). (B) Example of defects in the head skeleton, indicative of defects in head involution. (C) Example of complete failure of head involution. (D) Percentages of dead embryos in each phenotypic class for different allelic combinations of pyd alleles. (E–G) Central nervous system revealed by phalloidin staining for actin. pydMZ mutants do not exhibit obvious nervous system hypertrophy, although some had modest defects in axon architecture (G). Scale bars, 75 μm.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3113767&req=5

Figure 2: pydMZ mutants have defects in head involution but do not have serious deficits in Notch signaling. (A–C) Cuticles of pydMZ mutant embryos. (A) Example of wild-type phenotype, with intact head skeleton (arrow). (B) Example of defects in the head skeleton, indicative of defects in head involution. (C) Example of complete failure of head involution. (D) Percentages of dead embryos in each phenotypic class for different allelic combinations of pyd alleles. (E–G) Central nervous system revealed by phalloidin staining for actin. pydMZ mutants do not exhibit obvious nervous system hypertrophy, although some had modest defects in axon architecture (G). Scale bars, 75 μm.
Mentions: As a first assessment of the embryonic processes affected by Pyd loss, we examined the cuticles of mutant embryos at the end of embryogenesis. The cuticle is secreted by epidermal cells and provides a clear readout of cell fate choices and successful completion of morphogenetic movements. In wild-type embryos, cells of the head segments move forward and inward in a process called head involution and then secrete the specialized cuticle of the mouth parts (Figure 2A, arrow). At roughly the same time, lateral sheets of cells of the thoracic and abdominal epidermis move toward the dorsal midline, meeting and zipping closed in a process known as dorsal closure, resulting in an intact dorsal cuticle.

Bottom Line: Pyd loss does not dramatically affect AJ protein localization or initial localization of actin and myosin during dorsal closure.The defects, which include segmental grooves that fail to retract, a disrupted leading edge actin cable, and reduced zippering as leading edges meet, closely resemble defects in canoe zygotic mutants and in embryos lacking the actin regulator Enabled (Ena), suggesting that these proteins act together.Canoe (Cno) and Pyd are required for proper Ena localization during dorsal closure, and strong genetic interactions suggest that Cno, Pyd, and Ena act together in regulating or anchoring the actin cytoskeleton during dorsal closure.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of North Carolina at Chapel Hill, USA.

ABSTRACT
Adherens and tight junctions play key roles in assembling epithelia and maintaining barriers. In cell culture zonula occludens (ZO)-family proteins are important for assembly/maturation of both tight and adherens junctions (AJs). Genetic studies suggest that ZO proteins are important during normal development, but interpretation of mouse and fly studies is limited by genetic redundancy and/or a lack of alleles. We generated alleles of the single Drosophila ZO protein Polychaetoid (Pyd). Most embryos lacking Pyd die with striking defects in morphogenesis of embryonic epithelia including the epidermis, segmental grooves, and tracheal system. Pyd loss does not dramatically affect AJ protein localization or initial localization of actin and myosin during dorsal closure. However, Pyd loss does affect several cell behaviors that drive dorsal closure. The defects, which include segmental grooves that fail to retract, a disrupted leading edge actin cable, and reduced zippering as leading edges meet, closely resemble defects in canoe zygotic mutants and in embryos lacking the actin regulator Enabled (Ena), suggesting that these proteins act together. Canoe (Cno) and Pyd are required for proper Ena localization during dorsal closure, and strong genetic interactions suggest that Cno, Pyd, and Ena act together in regulating or anchoring the actin cytoskeleton during dorsal closure.

Show MeSH