31% of sogP129D/sogYL26 flies survive to adulthood. Of these, 15% exhibit partial loss of the posterior crossvein and the rest show more subtle alterations in which the posterior crossvein appears as a fragmented line. Only 12% of sogP129D/sogP1 transheterozygotes survive to adulthood and 46% of these exhibit various degrees of loss of the posterior crossvein.
80% of homozygous embryos survive to adulthood.
Homozygous viable, few flies transheterozygous with lethal sog alleles survive.
sogP129D, zen1 has lethal | recessive | embryonic stage phenotype
sogP129D is a suppressor of phenotype of tldunspecified
MadES1/Mad[+], sogP129D has filzkorper phenotype
MadES1/Mad[+], sogP129D has embryonic head phenotype
MadES1/Mad[+], sogP129D has amnioserosa phenotype
sogP129D, zen1 has embryonic/first instar larval cuticle phenotype
MadES1, sogP129D has filzkorper phenotype
MadES1, sogP129D has embryonic head phenotype
MadES1, sogP129D has amnioserosa phenotype
Only 39% of sogP129D/+ embryos derived from MadES1/+ females survive to adulthood. sogP129D embryos derived from MadES1/+ females have internalised filzkorper and lack head elements, indicative of weak ventralisation. The amnioserosa is reduced. sogP129D ; zen1 double mutant embryos die with a partially ventralised phenotype at 25oC.
Weak sog mutation.