The pigmentation mutation speck is a commonly used recombination marker characterized by a darkly pigmented region at the wing hinge. Identified in 1910 by Thomas Hunt Morgan, speck was characterized by Sturtevant as the most "workable" mutant in the rightmost region of the second chromosome and eventually localized to 2-107.0 and 60C1-2. Though the first speck mutation was isolated over 110 years ago, speck is still not associated with any gene. Here, as part of an undergraduate-led research effort, we show that speck is encoded by the Arylalkylamine N-acetyltransferase 1 (AANAT1) gene. Both alleles from the Morgan lab contain a retrotransposon in exon 1 of the RB transcript of the AANAT1 gene. We have also identified a new insertion allele and generated multiple deletion alleles in AANAT1 that all give a strong speck phenotype. In addition, expression of AANAT1 RNAi constructs either ubiquitously or in the dorsal portion of the developing wing generates a similar speck phenotype. We find that speck alleles have additional phenotypes, including ectopic pigmentation in the posterior pupal case, leg joints, cuticular sutures and overall body color. We propose that the acetylated dopamine generated by AANAT1 decreases the dopamine pool available for melanin production. When AANAT1 function is decreased, the excess dopamine enters the melanin pathway to generate the speck phenotype.

speck, First Identified in Drosophila melanogaster in 1910, Is Encoded by the Arylalkalamine N-Acetyltransferase (AANAT1) Gene.

The pigmentation mutation speck is a commonly used recombination marker characterized by a darkly pigmented region at the wing hinge. Identified in 1910 by Thomas Hunt Morgan, speck was characterized by Sturtevant as the most “workable” mutant in the rightmost region of the second chromosome and eventually localized to 2-107.0 and 60C1-2. Though the first speck mutation was isolated over 115 years ago, speck is still not associated with any gene. Here, as part of an undergraduate-led research effort, we show that speck is encoded by the Arylalkylamine N-acetyltransferase 1 (AANAT1) gene. Both alleles from the Morgan lab contain a retrotransposon in exon 1 of the RB transcript of the AANAT1 gene. We have also identified a new insertion allele and generated multiple deletion alleles in AANAT1 that all give a strong speck phenotype. In addition, expression of AANAT1 RNAi constructs either ubiquitously or in the dorsal portion of the developing wing generates a similar speck phenotype. We find that speck alleles have additional phenotypes, including ectopic pigmentation in the posterior pupal case, leg joints, cuticular sutures and overall body color. We propose that the acetylated dopamine generated by AANAT1 decreases the dopamine pool available for melanin production. When AANAT1 function is decreased, the excess dopamine enters the melanin pathway to generate the speck phenotype.

https://www.biorxiv.org/content/biorxiv/early/2019/10/13/800391.full.pdf

speck, first identified in Drosophila melanogaster in 1910, is encoded by the Arylalkalamine N-acetyltransferase (AANAT1) gene

ABSTRACT Genetic screens are used in Drosophila melanogaster to identify genes key in the regulation of organismal development and growth. These screens have defined signalling pathways necessary for tissue and organismal development, which are evolutionarily conserved across species, including Drosophila. Here, we have used an FLP/FRT mosaic system to screen for conditional regulators of cell growth and cell division in the Drosophila eye. The conditional nature of this screen utilizes a block in the apoptotic pathway to prohibit the mosaic mutant cells from dying via apoptosis. From this screen, we identified two different mutants that mapped to the Hedgehog signalling pathway. Previously, we described a novel Ptc mutation and here we add to the understanding of disrupting the Hh pathway with a novel allele of Cos2. Both of these Hh components are negative regulators of the pathway, yet they depict mutant differences in the type of overgrowth created. Ptc mutations lead to overgrowth consisting of almost entirely wild-type tissue (non-autonomous overgrowth), while the Cos2 mutation results in tissue that is overgrown in both the mutant and wild-type clones (both autonomous and non-autonomous). These differences in tissue overgrowth are consistent in the Drosophila eye and wing. The observed difference is correlated with different deregulation patterns of pMad, the downstream effector of DPP signalling. This finding provides insight into pathway-specific differences that help to better understand intricacies of developmental processes and human diseases that result from deregulated Hedgehog signalling, such as basal cell carcinoma.

https://www.tandfonline.com/doi/pdf/10.1080/19336934.2022.2062991?needAccess=true

Patched and Costal-2 mutations lead to differences in tissue overgrowth autonomy

The mutation I.3.2 was previously identified in a FLP/FRT screen of chromosome 2R for conditional growth regulators. Here we report the phenotypic characterization and genetic mapping of I.3.2 by undergraduate students participating in Fly-CURE, a pedagogical program that teaches the science of genetics through a classroom research experience. We find that creation of I.3.2 cell clones in the developing eye-antennal imaginal disc causes a headless adult phenotype, suggestive of both autonomous and non-autonomous effects on cell growth or viability. We also identify the I.3.2 mutation as a loss-of-function allele of the gene centromere identifier ( cid ), which encodes centromere-specific histone H3 variant critical for chromosomal segregation.

The I.3.2 developmental mutant has a single nucleotide deletion in the gene centromere identifier

Genetic screens have been used to identify genes involved in the regulation of different biological processes. We identified growth mutants in a Flp/FRT screen using the Drosophila melanogaster eye to identify conditional regulators of cell growth and cell division. One mutant identified from this screen, B.2.16, was mapped and characterized by researchers in undergraduate genetics labs as part of the Fly-CURE. We find that B.2.16 is a non-lethal genetic modifier of the Dark82 mosaic eye phenotype.

https://www.micropublication.org/pdf/micropub-biology-000359

B.2.16 is a non-lethal modifier of the Dark82 mosaic eye phenotype in Drosophila melanogaster.

Genetic mapping of shn in Drosophila melanogaster Kayla Bieser1, Jamie Siders Sanford2, Ken Saville3, Katherine F. Arreola1, Zachary T. Ayres2, David Basulto1, Serena Benito1, Christopher J. Breen3, Julian A. Brix1, Nicole Brown1, Krissa K. Burton2, Taree M. Chadwick1, Matthew Chen3, Katherine Chu1, Beverly L. Corbett1, Zerick Dill3, Meghan A. Faughender1, Ashlynn D. Hickey2, Joshua S. Julia2, Shannon S. Kelty2, Brigette B. K. Kobs3, Bryce A. Krason1, Brian Lam1, Colin L. McCullough2, Bryanna R. McEwen2, Julian L. McKenzie2, Kayla R. McQuinn3, Chloe M. Moritz2, Kristina E. Myers2, Elizabeth M. Naugle2, Ashley M. Nutter2, Danielle Q. O’Conke2, Megan T. O’Grondik2, Kriya B. Patel2, Sydney M. Rudowski3, Emma N. Sberna2, Gunner M. Stall3, Tad L. Steiner2, Eda Tanriverdi2, Natalia Torres Patarroyo1, Virginia L. Traster1, Leo P. Tsai1, Andrew J. Valenti2, Mariela M. Villegas1, Samantha M. Voors2, Kierra K. Watson2, Megan E. Wright2, and Jacob D. Kagey4# #corresponding author 1. Department of Physical and Life Sciences, Nevada State College 2. Department of Biological and Allied Health Sciences, Ohio Northern University 3. Department of Biology, Albion College 4. Biology Department, University of Detroit Mercy

https://www.micropublication.org/media/2019/06/Bieser-2019.06.14.pdf

Zerrick Dill

Papers

Genetic mapping of shnE.3.2 in Drosophila melanogaster.