Action potentials recorded from the ab3 sensilla of 'Δhalo' (Df(2L)dp-79b/Dp(2;2)dpp^d21) flies show complete absence of large amplitude spikes when challenged with insect repellent odorants DEET, IR3535 or picaridin.

The synthetic deletion created using Df(2L)dp-79b and Dp(2;2)dpp^d21 recombined onto the same chromosome (see FBrf0173068 and FBrf0159257) deletes Or22a and Or22b, resulting in antennal olfactory receptor neuron ab3A losing its odorant response. This genetic background is referred to as "Δab3A".

Animals homozygous for the synthetic deletion created using Df(2L)dp-79b and Dp(2;2)dpp^d21 combined on to the same chromosome (see FBrf0173068 and FBrf0159257) constitute the 'empty neuron system', in which antennal olfactory receptor neuron ab3A loses its odorant response.

Animals homozygous for the synthetic deletion called "Δhalo" (in which Df(2L)dp-79b and Dp(2;2)dpp^d21 are recombined onto the same chromosome) have abnormal antennal electrophysiology: the ab3A neurons are unresponsive to a large panel of odours, in contrast to wild type. The ab3B neurons in the mutant flies show an odour response spectrum similar to that of wild-type flies, except that the response to pentyl acetate is greater than that of controls. Some mutant ab3A neurons show a low level of activity that consists largely of bursts of action potentials. These bursts typically contain 3 or 4 action potentials, with an interspike interval of 14 +/- 0.8 ms and occur at approximately 10 second intervals in the absence of odour stimulation. The frequency of bursts increases during responses of the neighbouring ab3B neuron, but the overall frequency of firing is still very low. All other neuronal classes in large basiconic sensilla of the antenna appear normal, as judged by testing them with the odours against which they normally respond most strongly. The ab3A neurons in "Δhalo" animals target the DM2 glomerulus as occurs in wild-type animals and there are no gross abnormalities in projections.

Embryos homozygous for the synthetic deletion termed "Δ(halo)" (in which Df(2L)dp-79b and Dp(2;2)dpp^d21 are recombined onto the same chromosome) fail to exhibit cytoplasmic clearing of lipid droplets. The physical parameters of droplet motion are altered in these mutants; in phase II of clearing, the stall forces are altered in both plus-end and minus-end directed motion, resulting in unbalanced forces. This leads to a net plus-end directed transport of the droplets.

The injection of halo^cGa RNA into embryos homozygous for "Δ(halo)" (in which Df(2L)dp-79b and Dp(2;2)dpp^d21 are recombined onto the same chromosome) partially rescues the cytoplasmic lipid drop clearing phenotype seen in these embryos. When embryos are injected in phase II, noticeable clearing is observed towards the end of phase II. and clouding fails to occur near the injection site.

The deletion 'Δhalo' is a synthetic deficiency that combines Df(2L)dp-79b and Dp(2;2)dpp^d21 (see FBrf0173068).

The combination of aberrations Df(2L)dp-79b Dp(2;2)dpp^d21 is referred to as "Or22a/b^Δhalo".

The combination of aberrations Df(2L)dp-79b/Dp(2;2)dpp^d21 is referred to as 'Δhalo'.