The Drosophila melanogaster otherwise known as a common fruit fly serves as a novel organism for genetic study. By studying mutations in Drosophila melanogaster researchers can better understand how the processes of Mendelian Genetics are implored in organisms and subsequently in humans. The purpose of this paper is to describe the phenotypic differences of Wild-type Drosophila melanogaster with a given mutant as well as attempt to recognize the mutation as one of five gene mutations. The mutation provided was number 510. Upon first examination this mutation appeared not to have wings, which led to our team giving the nick-name crawler. Male and female Drosophila melanogaster were both similarly affected by the mutation and it was noticeable from the moment of eclosion. Other physical differences that were noticed were that the crawler mutant lacked halteres. Also observed was that the development of the mutant from embryo to adult occurred faster than that of the WT. The WT would go through the cycle in approximately 10 days while the mutant crawler can complete its cycle in 7-8 days. The stages of egg, larva and pupa formation were noted as physically looking the same as the WT. Newly eclosed flies also looked similar in all facets besides missing the wings and halteres . Additionally, some mutants express different levels of the crawler mutations as some specimen have small nubs in the place of their wings, while others are completely wingless. The mutation was shown to express reccesive inheritance after performing a reciprocal cross called WT1 cross of WT virgin females with the crawler mutant males. The progeny obtained were shown to be WT flies (with wings) proving the mutation is recessive.
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By conducting research through use of an online database the possible mutations were narrowed down into five categories. wingless was the first of five that could potentially be the ‘crawler’ mutation. The wingless mutation, wg, is a protein coding gene located on the second chromosome linked to the chromosome on the twenty-five cM (centimorgans) from the centromere (2-25) (Thurmond J et al. 2019). The wg mutant is related to winglessness by encoding for a ligand of the Wnt/Wg ( Wingless) signaling pathway, which subsequently is monitored by the hemocyte differentiation in Drosophila melanogaster . (Sinenko et al. 2009).
Another possibility is the earthbound 1 or ebd1; a recessive protein coding gene. This mutation also makes the effected individual wingless as it promotes wg signaling. ebd1 is in the Centromere Binding Protein B binding domain protein family and through the use of genetic screen was shown to be a mutation that promotes wingless signaling. (Benchabane et al. 2011). This gene is located on the left arm of the third chromosome and is .5 cM from centromere ( 3-0.5) (Thurmond J et al. 2019).
The armadillo or arm protein coding gene is another possible mutation. This genes location on the recombination map is 1-0.2 meaning it is on the first ‘X’ chromosome, only 0.2 cM from the centromere, as well being a recessive mutation (Thurmond J et al. 2019). armadillo ‘s function is heavily related to he wingless signal transduction pathway as well as in the neural and memory pathways of Drosophila melanogaster. ( Loureiro 1998)
The mutation for sulfateless ( sfl) is a recessive protein coding gene that dramatically reduces the amount of Heparan Sulfate (HS) in Drosophila melanogaster during development thus increasing the chances of wingless progeny. Upon further inspection of HS winglessness was proven to be on a gradient which supports the theory that some crawler mutants have different levels of wing morphology. (Baeg, G.H et al. 2004). The mutation sfl is located on the left arm of the third chromosome, approximately 17 cM from the centromere (3-17) (Thurmond J et al. 2019).
Lastly, the porcupine or por is a recessivemutation that functions in the endoplasmic reticulum of Drosophila melanogaster. Expression of por enacts N-glycosylation which subsequently will challenges the normal wing gene and compete for spots thus can cause the progeny to not have wings. (Tanaka, K et al. (2002).) por is located on the first chromosome, sixty cM away from the centromere ( 1-60). According to the sequence location it is also located on the X chromosome (Thurmond J et al. 2019).
Drosophila melanogaster Wild-Type & Mutant ‘crawler’ – Figure 1
A(Thurmond J et al. 2019)C
B(Thurmond J et al. 2019)C
Figure 1. Contains images of the mutant male (crawler) on the right hand (Labeled B) side as well as the WT male on the left panel. (Labeled A)
A. Wild-Type: The WT male shows all the normal body parts of a Drosophila melanogaster. The entirety of the wing can be seen connected to the thorax (1) , as well as the halteres between the thorax and abdomen. (2)
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B. (crawler) Mutant: Unlike the WT phenotypethe male mutant is shown to be missing his wings (3) as well as the halteres (4). The scutellum remains identical, including the scutellar bristles. There are no other visible physical differences between the mutant and WT phenotypes.
References and Citations
- Baeg, G.H., Lin, X., Khare, N., Baumgartner, S., Perrimon, N. (2001). Heparan sulfate proteoglycans are critical for the organization of the extracellular distribution of Wingless. Development 128(1): 87–94.
- Benchabane, H., Xin, N., Tian, A., Hafler, B.P., Nguyen, K., et al(2011). Jerky/Earthbound facilitates cell-specific Wnt/Wingless signalling by modulating β-catenin-TCF activity. EMBO J. 30(8): 1444–1458.)
- Loureiro J, Peifer M. Roles of Armadillo, a Drosophila catenin, during central nervous system development. Curr Biol. 1998 May 21;8(11):622-32. doi: 10.1016/s0960-9822(98)70249-0. PubMed PMID: 9635189.
- Tanaka, K., Kitagawa, Y., Kadowaki, T. (2002). Drosophila segment polarity gene product porcupine stimulates the posttranslational N-glycosylation of wingless in the endoplasmic reticulum. J. Biol. Chem. 277(15): 12816–12823.
- Thurmond J, Goodman JL, Strelets VB, Attrill H, Gramates LS, et al and the FlyBase Consortium. (2019) FlyBase 2.0: the next generation. Nucleic Acids Res. 47(D1) D759–D765
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