Gene Dmel\elav

Embryonic lethal, or in the case of viable and ostensibly hypomorphic alleles, displays poor jumping and flying ability plus aberrant visual physiology and behavior. No morphological abnormalities visible in sections of dying embryos (elav1, elav2, or elav3); however, whole-mount embryos show periodic interruptions in the longitudinal connectives of the CNS and missing commissures especially the posterior ones (Jimenez and Campos-Ortega). elavts1 allows survival to adult stage at 19-25 but viability is reduced and adults usually die soon after eclosion; viability after rearing at 30 is very low and newly emerged adults show poor coordination and die soon; this temperature-sensitive allele also causes morphological abnormalities in the brain, especially in the visual system (after postembryonic shift from 19 to 30 or even following all development at low-temperature); optic chiasma is abnormal and second order optic lobe (medulla) is rotated to aberrant position (Campos et al., 1985); when elavts1 raised at 30, surface of eye is rough and photoreceptor layer abnormal in sections (Campos et al., 1985). Another temperature-sensitive allele elav19 also induces abnormalities of visual system (Homyk et al., 1985); rearing at 29 or high-temperature pulses delivered to pupae, raised otherwise at 20, causes vacuolization of photoreceptors and disorganization of rhabdomeres; high-temperature rearing or pupal pulsing induces severe optic lobe defects (absence of size reduction); electroretinograms of this mutant, raised at high-temperature, are missing light-on and light-off transient spikes (also seen after low-temperature rearing) and have reduction of ERG photoreceptor potential; amplitude of this potential also deteriorates as does deep pseudopupil when adults treated at high-temperature after low-temperature rearing; mosaic analysis (Campos et al., 1985) of elav1 reveals autonomously induced defects in eye morphology, but no effects on other imaginal disc derivatives, and suggests both directly induced defects in optic lobe development, as well as inductively caused CNS defects mediated through expression of this mutation in the eye (i. e., such that the visual system's ganglia are genotypically normal). Lethal "focusing" in these mosaics suggests influence of gene on derivatives of ventral blastoderm. In studies of viable alleles, elav19 and elav20, both of which are temperature-sensitive, flying and jumping ability shown to be especially aberrant after rearing at 29; wing position also aberrant; elavts1 most severe, including having no optomotor response when raised at high (or even low) temperature; temperature-sensitive period for aberrant wing posture in elav19 extends from larval to pupal period (Homyk and Grigliatti). An antibody specific to neuronal nuclei fails to stain neurons of elav-deficient embryos; however, the quantity of antigen does not respond to the number of elav+ genes present (Bier, Ackerman, Barbel, Jan and Jan, 1988, Science 240: 913-16). elav transcripts detected in all postmitotic neurons, from their birth; not seen in embryonic or larval neuroblasts. Also seen in larval eye discs, adult retinas and Johnston's organ of the antennae.