Conserved Domains of the Nullo Protein Required for Cell-Surface Localization and Formation of Adherens Junctions

Hunter, Christine; Sung, Patricia; Schejter, Eyal D.; Wieschaus, Eric

doi:10.1091/mbc.01-08-0418

Cited by 24 publications

(22 citation statements)

References 42 publications

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“…To get around this problem we have made use of the effects of nullo protein. Expression of nullo during late cellularization completely blocks the formation of apical spot junctions (Hunter et al, 2002;Hunter and Wieschaus, 2000). To confirm that results using this technique are due to the lack of adherens junctions and not to additional effects of nullo expression we repeated the analysis with embryos made from arm 043A01 germline clones.…”

Section: Translating Myosin Localization Into Cell Shape Change -The mentioning

confidence: 98%

folded gastrulation, cell shape change and the control of myosin localization

et al. 2005

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The global cell movements that shape an embryo are driven by intricate changes to the cytoarchitecture of individual cells. In a developing embryo,these changes are controlled by patterning genes that confer cell identity. However, little is known about how patterning genes influence cytoarchitecture to drive changes in cell shape. In this paper, we analyze the function of the folded gastrulation gene (fog), a known target of the patterning gene twist. Our analysis of fog function therefore illuminates a molecular pathway spanning all the way from patterning gene to physical change in cell shape. We show that secretion of Fog protein is apically polarized, making this the earliest polarized component of a pathway that ultimately drives myosin to the apical side of the cell. We demonstrate that fog is both necessary and sufficient to drive apical myosin localization through a mechanism involving activation of myosin contractility with actin. We determine that this contractility driven form of localization involves RhoGEF2 and the downstream effector Rho kinase. This distinguishes apical myosin localization from basal myosin localization, which we find not to require actinomyosin contractility or FOG/RhoGEF2/Rho-kinase signaling. Furthermore, we demonstrate that once localized apically, myosin continues to contract. The force generated by continued myosin contraction is translated into a flattening and constriction of the cell surface through a tethering of the actinomyosin cytoskeleton to the apical adherens junctions. Our analysis of fog function therefore provides a direct link from patterning to cell shape change.

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Section: Translating Myosin Localization Into Cell Shape Change -The mentioning

confidence: 98%

folded gastrulation, cell shape change and the control of myosin localization

et al. 2005

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“…S3). We also made a rescue construct of dunk, in which the expression of full-length dunk coding sequence plus a C-terminal 3×HA tag is under the control of the nullo promoter (P nullo ; Hunter et al, 2002). Dunk-3HA showed similar localization as endogenous Dunk and rescued the myosin phenotype in dunk 1 mutant embryos (Fig.…”

Section: Myosin Flow Is Misdirected In Dunk Mutant Embryosmentioning

confidence: 99%

Flow-dependent myosin recruitment during Drosophila cellularization requires zygotic dunk activity

He¹,

Martin²,

Wieschaus³

2016

Journal of Cell Science

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Actomyosin contractility underlies force generation in morphogenesis ranging from cytokinesis to epithelial extension or invagination. In Drosophila, the cleavage of the syncytial blastoderm is initiated by an actomyosin network at the base of membrane furrows that invaginate from the surface of the embryo. It remains unclear how this network forms and how it affects tissue mechanics. Here, we show that during Drosophila cleavage, myosin recruitment to the cleavage furrows proceeds in temporally distinct phases of tension-driven cortical flow and direct recruitment, regulated by different zygotic genes. We identify the gene dunk, which we show is transiently transcribed when cellularization starts and functions to maintain cortical myosin during the flow phase. The subsequent direct myosin recruitment, however, is Dunk-independent but requires Slam. The Slam-dependent direct recruitment of myosin is sufficient to drive cleavage in the dunk mutant, and the subsequent development of the mutant is normal. In the dunk mutant, cortical myosin loss triggers misdirected flow and disrupts the hexagonal packing of the ingressing furrows. Computer simulation coupled with laser ablation suggests that Dunk-dependent maintenance of cortical myosin enables mechanical tension build-up, thereby providing a mechanism to guide myosin flow and define the hexagonal symmetry of the furrows.

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“…The nulloX (X) embryos were collected from the C(1)DX, ywf stock (Wieschaus and Sweeton, 1988). The cellularization phenotypes of these nulloX embryos were rescued with a nullo transgene (Hunter et al, 2002;Rose and Wieschaus, 1992). For live imaging, the stock C(1)DX, ywf; Spider-GFP was prepared by making the insertion 95-1 spider-GFP (III; Gavdos Protein Trap, Observatoire Océanologique, Villefranche-sur-mer, France) homozygous in C(1)DX, ywf.…”

Section: Flies and Geneticsmentioning

confidence: 99%

Zygotically controlled F-actin establishes cortical compartments to stabilize furrows duringDrosophilacellularization

Sokac

Wieschaus

2008

Journal of Cell Science

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Cortical compartments partition proteins and membrane at the cell surface to define regions of specialized function. Here we ask how cortical compartments arise along the plasma membrane furrows that cellularize the early Drosophila embryo, and investigate the influence that this compartmentalization has on furrow ingression. We find that the zygotic gene product Nullo aids the establishment of discrete cortical compartments, called furrow canals, which form at the tip of incipient furrows. Upon nullo loss-of-function, proteins that are normally restricted to adjacent lateral regions of the furrow, such as Neurotactin and Discs large, spread into the furrow canals. At the same time, cortical components that should concentrate in furrow canals, such as Myosin 2 (Zipper) and Anillin (Scraps), are missing from some furrows. Depletion of these cortical components from the furrow canal compartments precipitates furrow regression. Contrary to previous models, we find that furrow compartmentalization does not require cell-cell junctions that border the furrow canals. Instead, compartmentalization is disrupted by treatments that reduce levels of cortical F-actin. Because the earliest uniform phenotype detected in nullo mutants is reduced levels of F-actin at furrow canals, we propose that Nullo compartmentalizes furrows via its regulation of Factin, thus stabilizing furrows and insuring their ingression to complete cellularization. Supplementary material available online at

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Conserved Domains of the Nullo Protein Required for Cell-Surface Localization and Formation of Adherens Junctions

Cited by 24 publications

References 42 publications

folded gastrulation, cell shape change and the control of myosin localization

folded gastrulation, cell shape change and the control of myosin localization

Flow-dependent myosin recruitment during Drosophila cellularization requires zygotic dunk activity

Zygotically controlled F-actin establishes cortical compartments to stabilize furrows duringDrosophilacellularization

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