Genetic control in drosophila patterning
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- Wikipedia article: Morphogenesis
Genes Required for Embryonic Patterning
Identification of Embryonic Patterning Genes
The genes required for embryonic patterning were identified by Christiane Nüsslein-Volhard and Eric Wieschaus through use of random saturation mutagenesis experiments. Mutations that caused abnormal array of cuticle structures and embryonic lethality were kept for study. The screen below was used to identify second chromosome mutations that effect embryonic patterning.
The * marks a chromosome treated with mutagen, it does not necessarily mean a mutation has occurred. If there are no white eyed progeny, this is a lethal mutation. Eggs were collected and cuticle was analyzed for pattern defects.
Balancer chromosomes like CyO have multiple inversions and a dominant visible marker. Sy suppressing recombination, they keep linked mutations together and allow mutagenized chromosomes to be followed. CyO is also homozygous lethal and will kill unwanted homozygous flies in the G2.
A chromosome carrying a dominant temperature sensitive (DTS) mutation is also used here to kill unwanted flies in the G2.
It was discovered that two classes of mutations affect embryonic patterning: maternal effect and zygotic letha mutations. The screen identified 120 genes in the total genome that are zygotically essential for embryonic pattern formation.
How is the pattern established?
Maternal effect genes
For maternal effect genes, the genotype of the mother determines the phenotype of the offspring. Maternal genes initiate anterior/posterior pattern.
female m/m x +/+ male ---------> all mutant embryos
female m/+ x m/+ male ---------> no mutant embryos
35 maternal effect genes were identified that are required for normal embryonic patterning. Maternal effect gene products are transported into egg from germline nurse cells.
Bicoid RNA is transcribed in nurse cells of the ovary. Nurse cells dump their contents into the anterior of the oocyte; bicoid RNA sticks at the site where it enters the oocyte. After egg laying, bicoid protein is synthesized, and diffuses to make a gradient in the anterior 70% of the embryo.
The bicoid protein is a transcription factor that promotes the transcription of the gap gene hunchback in the anterior part of the embryo.
Posterior Pole Plasm
The posterior pole plasm is a classic example of a localized, maternal cytoplasmic determinant. Transplantation of pole plasm showed that it is sufficient for the formation of functional pole cells.
At least two RNAs (oskar and nanos) and two proteins (vasa and staufen) are localized in the pole plasm in polar granules. Like bicoid RNA, nanos RNA is localized through binding of its 3' UTR to a pole of the oocyte (the posterior pole). After fertilization, nanos RNA is translated and the nanos protein forms a gradient that allows abdominal development. Unlike bicoid, nanos proteins act post-transcriptionally. Nanos protein destroys maternal hunchback RNA which would otherwise block abdominal development.