Amino acid replacement: V1055S. Amino acid replacement: T?I.
C7594597T
T1087I | scra-PA; T1114I | scra-PB
T?I
Position of mutation on reference sequence inferred by FlyBase curator based on Figure 1 of FBrf0187458. A Val to Ser change at the beginning of the PH domain (V1080 of scra-PA) is present in all Schupach/Wieschaus alleles sequenced. May be a polymorphism.
Females, homozygous for scra5, lay morphologically normal eggs that fail to hatch. These mutant embryos exhibit cellularisation defects. In embryos from scra5/scra4 mothers, early furrow canals lack the characteristic `tear-drop' shape. As these embryos progress through cellularisation, the contractile rings fail to form. During gastrulation, the transition from a hexagonal network into contractile rings fails, with a broken, hexagonal mesh in place of the normal lattice of rings. The cellularisation front is disorganised and nuclei are mis-positioned, with the newly formed cells open at their bases. Despite defects in furrow canal structure and septin targeting, the cellularisation front still ingresses in scra5/scra1 mutant embryos. In comparison to wild-type, the initiation phase of ingression is eliminated. Instead, a cellularisation front begins to ingress as soon as mitosis is completed, at a roughly constant slow rate. A distinct transition to a faster rate can be observed, but both slow and fast rates of ingression are slower than their wild-type counterparts. As the cellularisation front ingresses, extensive abnormalities become apparent. Furrow canals are malformed, appearing narrow or absent. Embryos in slow phase exhibit both paired plasma membranes and lines of vesicles in different areas of the same specimen, while those embryos in fast phase exhibit only lines of vesicles, in place of paired plasma membranes between nuclei. In scra5/scra1-derived embryos the pole cells are properly formed and enclosed by intact spherical plasma membranes, as in wild-type.
Cellularizing embryos from scra4/scra5 mothers lack the microfilament rings seen at the base of furrow canals in wild-type embryos at this stage. The furrow canals themselves are collapsed and lack the early bulb-like or the late flask-like morphology of the wild type. Viewed from the embryo surface, the furrow canals are not round, as in wild-type, but are irregular in shape and sharply angular. The sides remain straight and show no waviness that would indicate a lack of tension.
Eggs derived from homozygous females form a syncytial blastoderm and begin to cellularise normally, but cellularisation is often not completed. Gastrulation takes place but is usually very abnormal. The embryos form pieces of cuticle. Homozygous viable, hemizygous lethal.
homozygous viable but lethal over the deficiency.
scra5/scra4 has furrow canal | maternal effect phenotype, suppressible | partially by Df(3R)tll-e
The basal openings of the furrow canals in cellularizing embryos from scra4/scra5; Df(3R)tll-e mothers are more contracted than in wild-type, despite the absence of microfilament rings. These contracted basal openings are almost round. (Note - unclear from text if interacting deficiency is maternal or zygotic.)
Based on adult viability, and common cellularisation defects, the following scra alleles can be ranked from strongest to weakest as follows: scra7 = scra8 > scra03427 > scra5 = scra4 > scra1 > scra3 = scra6 = scraB26-35 = scraC82-45.