Drosophila melanogaster
Lifecycle and reproduction

Under optimal growth conditions at 25 °C (77 °F), the D. melanogaster lifespan is about 50 days from egg to death. The developmental period for D. melanogaster varies with temperature, as with many ectothermic species. The shortest development time (egg to adult), 7 days, is achieved at 28 °C (82 °F). Development times increase at higher temperatures (11 days at 30 °C or 86 °F) due to heat stress. Under ideal conditions, the development time at 25 °C (77 °F) is 8.5 days, at 18 °C (64 °F) it takes 19 days and at 12 °C (54 °F) it takes over 50 days. Under crowded conditions, development time increases, while the emerging flies are smaller. Females lay some 400 eggs (embryos), about five at a time, into rotting fruit or other suitable material such as decaying mushrooms and sap fluxes. Drosophila melanogaster is a holometabolous insect, so it undergoes a full metamorphosis. Their life cycle is broken down into 4 stages: embryo, larva, pupa, adult. The eggs, which are about 0.5 mm long, hatch after 12–15 hours (at 25 °C or 77 °F). The resulting larvae grow for about 4 days (at 25 °C) while molting twice (into second- and third-instar larvae), at about 24 and 48 h after hatching. During this time, they feed on the microorganisms that decompose the fruit, as well as on the sugar of the fruit itself. The mother puts feces on the egg sacs to establish the same microbial composition in the larvae's guts that has worked positively for herself. Then the larvae encapsulate in the puparium and undergo a 4-day-long metamorphosis (at 25 °C), after which the adults eclose (emerge).

Drosophila melanogaster, commonly known as the fruit fly, has been a significant model organism in embryonic development research. Many of its genes that regulate embryonic development and their mechanisms of action have been crucial in understanding the fundamental principles of embryonic development regulation in many multicellular organisms, including humans. Here are some important genes regulating embryonic development in Drosophila melanogaster and their modes of action:

Maternal genes: These genes are encoded in the female fruit fly and are present in the early stages of embryo development. They determine the embryo's main features and early development. For example, the gene called Bicoid regulates the formation of the embryo's anterior end, and its absence leads to an embryo lacking a head.

Zygotic genes: These genes are activated in later stages of embryo development when the fruit fly embryo begins to produce its own genetic products. For example, the hunchback gene regulates the formation of segments in the embryo.

Homeotic genes: This gene family regulates segmentation and axial patterning in development. They act as regulatory factors that determine cell fate in embryonic development. For example, the gene called Antennapedia regulates the formation of anterior limbs in the embryo.

Morphogens: These are molecules that form gradients in embryonic development and regulate cell fate depending on their position in the gradient. For example, the Hedgehog morphogen regulates the differentiation of segments and segment identity in the fruit fly embryo.

These genes and their modes of action form a complex regulatory network that guides the embryonic development of Drosophila melanogaster. They influence cell differentiation, segment formation, and axial patterning in the embryo, ultimately leading to the development of a fully formed adult fruit fly.

Males perform a sequence of five behavioral patterns to court females. First, males orient themselves while playing a courtship song by horizontally extending and vibrating their wings. Soon after, the male positions himself at the rear of the female's abdomen in a low posture to tap and lick the female genitalia. Finally, the male curls his abdomen and attempts copulation. Females can reject males by moving away, kicking, and extruding their ovipositor. Copulation lasts around 15–20 minutes, during which males transfer a few hundred, very long (1.76 mm) sperm cells in seminal fluid to the female. Females store the sperm in a tubular receptacle and in two mushroom-shaped spermathecae; sperm from multiple matings compete for fertilization. A last male precedence is believed to exist; the last male to mate with a female sires about 80% of her offspring. This precedence was found to occur through both displacement and incapacitation. The displacement is attributed to sperm handling by the female fly as multiple matings are conducted and is most significant during the first 1–2 days after copulation. Displacement from the seminal receptacle is more significant than displacement from the spermathecae. Incapacitation of first male sperm by second male sperm becomes significant 2–7 days after copulation. The seminal fluid of the second male is believed to be responsible for this incapacitation mechanism (without removal of first male sperm) which takes effect before fertilization occurs. The delay in effectiveness of the incapacitation mechanism is believed to be a protective mechanism that prevents a male fly from incapacitating his own sperm should he mate with the same female fly repetitively. Sensory neurons in the uterus of female D. melanogaster respond to a male protein, sex peptide, which is found in semen. This protein makes the female reluctant to copulate for about 10 days after insemination. The signal pathway leading to this change in behavior has been determined. The signal is sent to a brain region that is a homolog of the hypothalamus and the hypothalamus then controls sexual behavior and desire. Gonadotropic hormones in Drosophila maintain homeostasis and govern reproductive output via a cyclic interrelationship, not unlike the mammalian estrous cycle. Sex peptide perturbs this homeostasis and dramatically shifts the endocrine state of the female by inciting juvenile hormone synthesis in the corpus allatum.

D. melanogaster is often used for life extension studies, such as to identify genes purported to increase lifespan when mutated. D. melanogaster is also used in studies of aging. Werner syndrome is a condition in humans characterized by accelerated aging. It is caused by mutations in the gene WRN that encodes a protein with essential roles in repair of DNA damage. Mutations in the D. melanogaster homolog of WRN also cause increased physiologic signs of aging, such as shorter lifespan, higher tumor incidence, muscle degeneration, reduced climbing ability, altered behavior and reduced locomotor activity.
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