Amino acid replacement: V57M. Mutation is at the C-terminal end of helix 1 in the hydrophobic core of the DNA-binding domain.
G18133912A
V57M | Hsf-PA; V57M | Hsf-PB; V57M | Hsf-PC; V57M | Hsf-PD
Hsf4 adults exhibit increased mortality upon heat induction when compared to controls.
Mutant flies show a reduced rate of survival compared to wild-type controls after infection with either Enterobacter cloacae, Listeria monocytogenes or Beauveria bassiana.
After a pre-heat shock at 36[o]C, Hsf4 mutants show substantial synaptic thermoprotection (as measured by the percentage of boutons responding) - thermoprotection is less than in pre-heat shocked wild type controls, but is greater than in Hsf4 mutants that did not receive a pre-heat shock treatment.
Flies show reduced resistance to heat stress compared to control flies.
Polytene chromosome puffs are absent after a shift to the non-permissive temperature.
Homozygotes are viable at temperatures of 25oC or below. Homozygotes arrest at the 1st or 2nd larval instar stage and die after 2-3 days without any further growth or development at the non-permissive temperature of 29oC. Viability is rescued in homozygous or hemizygous Hsf2/Df(2R)PclP2 flies carrying Hsf+t8. Homozygous adults show reduced survival after a 40 minute heat treatment at temperatures of 38oC and above, when compared to wild-type flies or homozygous Hsf4 flies carrying two copies of Hsf+t8. The temperature-sensitive period is at approximately 1.5-2.5 days of development. Homozygous adults are viable and fertile when kept at 29oC upon eclosion. Females mosaic for homozygous clones in the germ line are fertile at both permissive and restrictive temperatures.
Heat shock proteins are not synthesised in response to heat stress in adult homozygotes, in contrast to wild-type flies. Hsp70 synthesis is induced during recovery from anoxia, as in wild-type flies.