RNA helicase component of the male-specific lethal (MSL) histone acetyltransferase complex, a multiprotein complex essential for elevating transcription of the single X chromosome in the male (X chromosome dosage compensation) (PubMed:1653648, PubMed:25158899, PubMed:26545078). Within the MSL complex, the helicase activity of mle remodels roX non-coding RNA (roX1 and roX2)s to promote assembly of the MSL complex (PubMed:23870142, PubMed:26545078, PubMed:30649456, PubMed:30805612). Able to unwind blunt-ended RNA duplexes and has specificity for uridine-rich nucleotides (PubMed:26545078).

(UniProt, P24785)

Homozygous males die, but homozygous females survive. Males produced by homozygous females die during the third larval instar, whereas those produced by heterozygous females are late pupal lethals. Females transformed into phenotypic males (tra) or intersexes (dsx) unaffected by mle, i.e. mle acts only upon single-X-bearing flies. No interaction with msl-1 or msl-2 (Belote, 1983, Genetics 96: 165-86). mle4 males surviving at 18 are sterile, small, and slow developing. Concluded to be defective in dosage compensation in males based on decreased levels of X-linked-enzyme activities (G6PD, 6GPD, FUM, β-HAD) but not autosomally encoded enzymes (ADH, AO, GPDH, IDH) in homozygous mle4 male larvae and escaping adults, e.g. β-HAD. The incorporation of labeled uridine by the polytene X chromosome relative to that of 2R is lower than normal in mle4 males (Belote and Lucchesi, 1980, Nature 285: 573-75); steady-rate level of Sgs4 mRNA incompletely compensated in mle4 and mle4/mle6 male larvae (Breen and Lucchesi, 1986, Genetics 112: 483-91). Polytene X chromosome of mle males appears narrower and more densely stained than that of control males. Few homozygous mle gynandromorphs survive; XO patches small, with small bristles, and mostly confined to abdomen (Uenoyama, Uchida, Fukunaga, and Oishi, 1982, Genetics 102: 223-31). mle pole cell transplanted into wild-type hosts incapable of undergoing normal spermatogenesis (Bachiller and Sanchez, 1986, Dev. Biol. 118: 379-84). Homozygous (and to a lesser extent heterozygous) mle females that are heterozygous for SxlF1 (Uenoyama, Fukunaga, and Oishi, 1982, Genetics 102: 233-43; Skripsky and Lucchesi, 1982, Dev. Biol. 94: 153-64) or are the surviving progeny raised at 17 of homozygous da mothers (Cline, 1982, Genetics 100: 641-63) develop as intersexes.

Larvae or adults become rapidly paralyzed when exposed to 37 and rapidly recover on return to lower temperatures. Rearing stocks chronically at room temperature or above causes napts to "adapt" such that higher temperatures (> 40) are required for paralysis (Kyriacou and Hall, 1985). Experiments involving one-time rearing at low temperature caused napts to paralyze at relatively low temperatures (Nelson and Wyman, 1990). Axonal conduction (but not synaptic transmission) fails in larvae at high temperatures (Wu et al., 1978; Wu and Ganetzky, 1980), but action potentials in the giant fiber (GF) pathway of adults are not blocked at temperatures up to 43 (Elkins and Ganetzky, 1990; Nelson and Wyman, 1990), though the latency from brain stimulation to response of thoracic muscles are aberrantly long, even at low temperatures (Nelson and Wyman, 1990), and this long-latency disappears as the temperature is raised to 35 (Elkins and Ganetzky, 1990). "Following frequency" of napts thoracic muscle responses (re. GF pathway stimulation) reduced at elevated temperatures, an effect which can be reversed by injection of 4-amino-pyridine (Nelson and Wyman, 1990). At permissive temperatures, refractory period for elicitation of a series of action potentials is abnormally long (Ganetzky and Wu, 1980); at these low temperatures, napts suppresses effects of "hyperexcitability" mutations such as Sh, bas, bss, eas, Hk, kdn, and tko (Ganetzky and Wu, 1982, Genetics 100: 597-614). napts is unconditionally lethal (Ganetzky and Wu, 1980) in a double mutant with parats1 (death occurring during 1st larval instar) and the viability of other para; napts combinations is poor (Ganetzky, 1984); two doses of para+ (in males) suppresses high-temperature paralysis of napts (Stern et al., 1990). In mosaic experiments, cuticular clones of parats1 in a napts background (after low-temperature development) have non-functioning sensory cells, probably due to lack of nerve conduction which, however, did not cause any anatomical abnormalities involving the central projections of these sensory neurons (Burg and Wu, 1986). Another developmental study, examining larval nerve terminal innervating body-wall muscles (Budnik et al., 1990), showed slight reduction in the extent of branching caused by napts at permissive temperature; the increase in branching (and higher than normal number of varicosities on motor-neurites) induced by an eag Sh double mutant was suppressed by napts (re. low-temperature rearing). napts in combination with tipE leads to poor viability at permissive temperature for both mutants (Ganetzky, 1986, J. Neurogenet. 3: 19-31; Jackson, Wilson, and Hall, 1986, J. Neurogenet. 3: 1-17). napts is, at permissive temperature, hypersensitive to blocking effects of tetrodotoxin (TTX) on action potentials (Ganetzky and Wu, 1980); brain membrane extracts of napts, assayed at low or high temperatures, have subnormal levels of tetrodotoxin (Kauvar, 1982) or saxitoxin (Jackson et al., 1984) binding activity; the latter study reports that there are no qualitative alterations of this binding activity (kd is normal). Cultured neurons from napts larvae are 4 to 5-fold more resistant than wild-type cells to killing effects of veratridine, irrespective of temperature (22 vs 35) (Suzuki and Wu 1984, J. Neurogenet. 1: 225-38), but TTX has no effects on these mutant cells, whose general growth characteristics are also normal (Wu, Suzuki and Poo, 1983, J. Neurosci. 3: 1888-99). The mutation does not seem to modify the expression of sodium currents in embryonic neurons (O'Dowd and Aldrich, 1988, J. Neurosci. 8: 3633-43). Exposure of napts males to high temperature causes arrest of oscillator underlying rhythmic component of courtship song (Kyriacou and Hall, 1985); in experiments on conditioned courtship, napts males learn normally but have shortened memory spans, and napts suppresses Sh-induced decrements in courtship learning (Cowan and Siegel, 1984, J. Neurogenet. 1: 333-44; 1986, J. Neurogenet. 3: 187-201).