Df(3L)fz2 is homozygous lethal.

One copy of Df(3L)fz2 has no effect on hemocyte proliferation in third instar larvae.

The Df(3L)fz2 chromosome does not act as a dominant suppressor of telomeric silencing (assayed using the effect of the chromosome on the eye colour phenotype of flies carrying "P{w^var}KR3-2", a stable "brown-red" variant of the P{3'WP-2,w^var}2Lt insertion).

Homozygotes die shortly after hatching with subtly disorganized denticles in posterior compartments. Double mutants of fz²¹, fz²³ or Df(3L)fz-D21 with Df(3L)fz2 show variable embryonic segmentation defects ranging from a few extra denticles in the posterior part of some segments to complete replacement of naked cuticle with denticles. This phenotype is reminiscent of that for P{en1}wg^en11 loss of function. Double mutants of fz²¹ or fz²³ with Df(3L)fz2 show a complete loss (fz²¹) or reduction (fz²³) of RP2 neurons. In 21% of Df(3L)fz2 homozygotes an RP2 neuron is either missing or misplaced in 1-3 hemisegments. In double mutants of fz²¹ or fz²³ with Df(3L)fz2 cardiac precursors are missing. Double mutants of fz²¹ or fz²³ with Df(3L)fz2 lack the normal number of midgut constrictions. Overexpression of wg^UAS.cLb by Scer\GAL4^da.G32 has no effect on the cuticle phenotype of double mutants of fz²¹ or fz²³ with Df(3L)fz2.