arm3 maternal and zygotic embryonic mutants exhibit a fragmented cuticle.
Photoreceptor cell differentiation appears abnormal in arm3 mutant clones.
Embryos maternally and zygotically mutant for arm3 show weak staining for and improper localisation of the shg, arm and α-Cat gene products, suggesting little or no adherens junction formation.
Embryos maternally and zygotically mutant for arm3 contain cells of normal shape after cellularization. However, mutant embryos form a disorganized ventral furrow during early gastrulation and much of the ectoderm breaks into rounded, dissociated cells soon afterward. Nevertheless, cells make roughly correct cell fate choices, and some cells retain residual epithelial character and undergo limited morphogenesis.
Embryos maternally and zygotically mutant for arm3 form more epithelial folds than wild type embryos.
Cells in epithelial folds and rosettes of embryos maternally and zygotically mutant for arm3 are pear-shaped with a constricted and extended apical domain, whereas wild type epithelial cells adopt a columnar shape.
Basic cytoskeletal polarity appears to be maintained in the epithelial folds of embryos maternally and zygotically mutant for arm3, although actin and microtubules are disorganised in rounded dissociated mutant cells.
In embryos maternally and zygotically mutant for arm3, most neuroblasts fail to be internalized and divide laterally or orthogonally on the embryo surface, rather than in the apical-basal orientation as in wild type. However, as in wild type, neuroblasts divide asymmetrically and epithelial cells divide symmetrically in arm3 mutants.
arm3 maternal mutants have defects in spindle attachment to the cortex during syncytial divisions but do not have defects in pseudocleavage furrows. There is no evidence for multinucleate cells during cellularisation of arm3 maternal mutant embryos.
arm3 somatic stem cell (SSC) clones in the ovary are lost more rapidly than wild-type clones. Follicle cells in mutant clones do not have the wild-type regular columnar shape.
arm3 hemizygous embryos fail to form the second midgut constriction.
Leading edge cells fail to elongate uniformly in mutant embryos as dorsal closure is initiated.
Homozygous embryos derived from homozygous female germline clones show loss of nuclei from the surface of the embryo during syncytial development.
arm3/Y mutant cuticles are shorter than wild type, with a lawn of ventral denticles, no naked cuticle and incomplete dorsal closure. Embryos with a range of phenotypes is seen. In embryos with the most severe phenotype, the cuticle is much shorter than normal and is open dorsally. In less severe embryos, dorsal closure is partially complete and the cuticle is longer. At a very low frequency (0.5%), the cuticle is nearly wild type in length, has greater denticle diversity and is dorsally closed (the embryos retain an anterior hole).
Mutant embryos show dorsal closure defects and ventral defects revealed by loss of naked cuticle between denticle belts. At the end of germ band retraction the dorsal leading edge cells initiate cell shape cheanges, but in an uncoordinated fashion. A subset of more lateral cells fail to elongate. Most embryos fail to initiate dorsal closure and leading edge cells often curl under their more lateral neighbors. Amnioserosa eventually rips away from the leading edge cells with detached leading edge cells resuming a cuboidal shape.
Large follicle cell clones mutant for arm3 form a follicular epithelium. The mutant cells in most cases have a normal cuboidal to columnar shape.
Affected embryos show a strong segment polarity phenotype: reduced size, lawn of denticles and missing head structures.
All surviving ventral cells of hemizygous embryos secrete denticles.
Homozygotes show a strong zygotic segment polarity phenotype. Females with homozygous germlines can complete oogenesis, but homozygous embryos derived from these females are abnormal.
Embryos that are zygotically and maternally mutant for arm3 have a disrupted epithelium, and only patches of cuticle are secreted. The integrity of the cuticle is dramatically improved if these embryos are also expressing armS10.Scer\UAS.T:Hsap\MYC (using Scer\GAL4e22c), and the secreted cuticle is naked. The integrity of the cuticle is dramatically improved if these embryos are also expressing armS2.Scer\UAS.T:Hsap\MYC (using Scer\GAL4e22c), some of the secreted cuticle has denticles.
Germline mosaics cause failure in adhesion between follicle and germ cells in the egg chambers. Nurse cell cortical actin cytoskeleton is often disorganised with abnormal inclusions of actin present. Centripetal follicle cells frequently fail to migrate and separate the oocyte from the nurse cells and nurse cells often fail to transfer their contents into the oocyte. At a low frequency normal egg chambers are seen producing fertilizable eggs but egg production is greatly reduced. Of the eggs laid 23% are flat or half-filled. Of the full eggs 94% do not develop, the remaining 6% are fertilised and begin embryonic development. Half of the developing embryos arrest before secreting cuticle ("no cuticle" class). Deviation from normal development occurs before the cellular blastoderm stage. A quarter hatch or have a nearly normal cuticle ("wild-type" class). The remaining have a more dramatic cuticle phenotype secreting only a few cuticle scraps ("crumbs-like" class), due to lack of maternal and zygotic arm. Embryos cellularise normally but morphogenetic movements are disrupted at the onset of gastrulation, there is little or no germ band extension and the ventral furrow and posterior midgut fail to invaginate normally. Cell polarity is rapidly disrupted due to disruptions in adherens junctions. The epithelial monolayer of cells at the cellular blastoderm stage rapidly becomes a disordered, multilayered mesenchyme, the cells in this mesenchyme round up. Cell-cell adhesion is severely disrupted. "crumbs-like" class can be rescued by paternal arm correspondingly increasing the number of wild type embryos. Paternal arm cannot rescue the "no cuticle" class.
Females bearing germline clones lay some eggs, homozygous embryos develop normally, hemizygotes show poor differentiation of the larval cuticle. A rare class of hemizygotes shows very early defects, before and during cellularisation, due a disruption of zonula adherens formation. Other embryos develop normally until early gastrulation and then the monolayered epithelium becomes disordered and in some regions multilayered.
Embryos secrete only small portion of cuticle, due to disruption of adherens junction function.
Embryos arising from germ-line clones dissociate at the onset of gastrulation. Additional defects are evident in the egg and cellularization/early gastrulation of the embryo. Embryos deficient for both maternal and zygotic arm product have a crb like phenotype forming only scraps of cuticle.
Females with homozygous arm3 germlines lay eggs that are often flaccid, perhaps because residual nurse cells prevent proper closure of the egg cell at the anterior end. Those eggs that are laid have normal anterior-posterior and dorso-ventral patterning.
Homozygous clone tissue dies in the imaginal discs of larvae suggesting that arm+ activity is required in late larval and pupal stages.
Shows effects on segment polarity, head development and dorsal closure.