Drosophila Genetic Reference Panel

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Drosophila Genetic Reference Panel (DGRP) is a suite of Drosophila melanogaster lines derived from an out-crossed population in Raleigh, North Carolina. The founders of these lineages were collected from the Raleigh State Farmer's Market [1] 35°45′51″N78°39′47″W / 35.764254°N 78.662935°W / 35.764254; -78.662935 . The suite consists of 205 fully sequenced lines which have been inbred to near homozygosity. The primary goal of the DGRP is to provide a common set of strain for quantitative genetics research in Drosophila . Each researcher who uses the lines from the DGRP will have access to other researchers' data, which will be stored in a publicly available database. This allows for analyses to be performed across studies without having to worry about complications arising from different labs using genomically different lines of fruit flies. [2] [3]

Contents

Objectives

These lines are useful for performing QTL maps, as every line is fully sequenced. This allows for association mapping to be performed, which looks for genomic regions that are correlated to a phenotype. As labs produce QTL maps a comprehensive picture of the Drosophila genome will emerge with unprecedented resolution. Currently, dozens of quantitative traits are being examined by researchers, including longevity, phototaxis, mating behavior, wing morphology and oviposition site preference.

Current uses

The pilot proof of concept and development of the DGRP came from the Trudy Mackay lab in Raleigh, North Carolina. The sequencing was done by Baylor College of Medicine Sequencing Center, in collaboration with Richard Gibbs and Stephen Richards.

The preliminary sequence data can be obtained from a public database hosted by Baylor College of Medicine in the Texas Medical Center. [4] Raw sequencing data from the project can be found in the NCBI Sequence Read Archive. [5]

Specific studies

Preliminary data has been presented at Genetics Society of America in Boston, Massachusetts. The study investigates the sleep behavior of Drosophila to uncover the genes that are responsible. The data suggest that at least 998 genes are responsible for some of the measurable variation found, including candidate genes CrebB-17A , rutabaga , Shaker and the gene encoding the epidermal growth factor receptor have all been implicated in other studies as being involved in sleep behavior. [6]

Researchers have also uncovered a genotype by diet interaction that drives phenotypic variation. Recently published data indicates that the interaction between a fly's genome and its environment plays a substantial role in determining the phenotype. This suggests that some individuals are obese on a high-fat diet, but can retain a slimmer phenotype on a high-sugar diet. [7]

Related Research Articles

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<span class="mw-page-title-main">Human genome</span> Complete set of nucleic acid sequences for humans

The human genome is a complete set of nucleic acid sequences for humans, encoded as the DNA within each of the 24 distinct chromosomes in the cell nucleus. A small DNA molecule is found within individual mitochondria. These are usually treated separately as the nuclear genome and the mitochondrial genome. Human genomes include both protein-coding DNA sequences and various types of DNA that does not encode proteins. The latter is a diverse category that includes DNA coding for non-translated RNA, such as that for ribosomal RNA, transfer RNA, ribozymes, small nuclear RNAs, and several types of regulatory RNAs. It also includes promoters and their associated gene-regulatory elements, DNA playing structural and replicatory roles, such as scaffolding regions, telomeres, centromeres, and origins of replication, plus large numbers of transposable elements, inserted viral DNA, non-functional pseudogenes and simple, highly repetitive sequences. Introns make up a large percentage of non-coding DNA. Some of this non-coding DNA is non-functional junk DNA, such as pseudogenes, but there is no firm consensus on the total amount of junk DNA.

<span class="mw-page-title-main">Single-nucleotide polymorphism</span> Single nucleotide in genomic DNA at which different sequence alternatives exist

In genetics and bioinformatics, a single-nucleotide polymorphism is a germline substitution of a single nucleotide at a specific position in the genome. Although certain definitions require the substitution to be present in a sufficiently large fraction of the population, many publications do not apply such a frequency threshold.

<span class="mw-page-title-main">Mosaic (genetics)</span> Condition in multi-cellular organisms

Mosaicism or genetic mosaicism is a condition in which a multicellular organism possesses more than one genetic line as the result of genetic mutation. This means that various genetic lines resulted from a single fertilized egg. Mosaicism is one of several possible causes of chimerism, wherein a single organism is composed of cells with more than one distinct genotype.

A quantitative trait locus (QTL) is a locus that correlates with variation of a quantitative trait in the phenotype of a population of organisms. QTLs are mapped by identifying which molecular markers correlate with an observed trait. This is often an early step in identifying the actual genes that cause the trait variation.

Genetic architecture is the underlying genetic basis of a phenotypic trait and its variational properties. Phenotypic variation for quantitative traits is, at the most basic level, the result of the segregation of alleles at quantitative trait loci (QTL). Environmental factors and other external influences can also play a role in phenotypic variation. Genetic architecture is a broad term that can be described for any given individual based on information regarding gene and allele number, the distribution of allelic and mutational effects, and patterns of pleiotropy, dominance, and epistasis.

<span class="mw-page-title-main">Michael Ashburner</span> English biologist (1942–2023)

Michael Ashburner was an English biologist and Professor in the Department of Genetics at University of Cambridge. He was also the former joint-head and co-founder of the European Bioinformatics Institute (EBI) of the European Molecular Biology Laboratory (EMBL) and a Fellow of Churchill College, Cambridge.

A polygene is a member of a group of non-epistatic genes that interact additively to influence a phenotypic trait, thus contributing to multiple-gene inheritance, a type of non-Mendelian inheritance, as opposed to single-gene inheritance, which is the core notion of Mendelian inheritance. The term "monozygous" is usually used to refer to a hypothetical gene as it is often difficult to distinguish the effect of an individual gene from the effects of other genes and the environment on a particular phenotype. Advances in statistical methodology and high throughput sequencing are, however, allowing researchers to locate candidate genes for the trait. In the case that such a gene is identified, it is referred to as a quantitative trait locus (QTL). These genes are generally pleiotropic as well. The genes that contribute to type 2 diabetes are thought to be mostly polygenes. In July 2016, scientists reported identifying a set of 355 genes from the last universal common ancestor (LUCA) of all organisms living on Earth.

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A phene is an individual genetically determined characteristic or trait which can be possessed by an organism, such as eye colour, height, behavior, tooth shape or any other observable characteristic.

Paralytic is a gene in the fruit fly, Drosophila melanogaster, which encodes a voltage gated sodium channel within D. melanogaster neurons. This gene is essential for locomotive activity in the fly. There are 9 different para alleles, composed of a minimum of 26 exons within over 78kb of genomic DNA. The para gene undergoes alternative splicing to produce subtypes of the channel protein. Flies with mutant forms of paralytic are used in fly models of seizures, since seizures can be easily induced in these flies.

Population genomics is the large-scale comparison of DNA sequences of populations. Population genomics is a neologism that is associated with population genetics. Population genomics studies genome-wide effects to improve our understanding of microevolution so that we may learn the phylogenetic history and demography of a population.

Expression quantitative trait loci (eQTLs) are genomic loci that explain variation in expression levels of mRNAs.

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Nested association mapping (NAM) is a technique designed by the labs of Edward Buckler, James Holland, and Michael McMullen for identifying and dissecting the genetic architecture of complex traits in corn. It is important to note that nested association mapping is a specific technique that cannot be performed outside of a specifically designed population such as the Maize NAM population, the details of which are described below.

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A recombinant inbred strain or recombinant inbred line (RIL) is an organism with chromosomes that incorporate an essentially permanent set of recombination events between chromosomes inherited from two or more inbred strains. F1 and F2 generations are produced by intercrossing the inbred strains; pairs of the F2 progeny are then mated to establish inbred strains through long-term inbreeding.

<span class="mw-page-title-main">Abraham B Korol</span> Israeli geneticist

Abraham Bentsionovich Korol is a professor in the Institute of Evolution at the University of Haifa. He is a prominent Israeli geneticist and evolutionary biologist known for his work on the evolution of sex and recombination, genome mapping and the genetics of complex traits. Korol was born in Bendery city, Moldavia, then part of the Soviet Union, and immigrated to Israel in 1991. Before immigrating to Israel, Korol was appointed in 1981 as a senior researcher and was awarded the degree of Doctor of Science by the Presidium of Academy of Science USSR in 1988, and became a full professor in 1991. After immigrating to Israel in 1991, Korol has established and headed the Laboratory of Population Genetics and Computational Biology in the Institute of Evolution at the University of Haifa. He became full professor there in 1996 and served as the director of the Institute of Evolution between 2008 and 2013. Since 1994, Korol has filled many scholarly positions including member of the steering committee of Israeli Gene Bank; member of the Human Genome Organization; member of the European Society of Evolutionary Biology; a member of the Coordinating Committee of the International Wheat Genome Sequencing Consortium; member of the Infrastructure Steering Committee of the Israeli Ministry of Science; representative of Haifa University in the Kamea program steering committee ; member of the Advisory Committee of Absorption in Science of the Israeli Ministry of Absorption.

<span class="mw-page-title-main">Complex traits</span>

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References

  1. ↑ "NCDA&CS - Marketing Division - Raleigh Farmers Market". www.ncagr.gov.
  2. ↑ Archived 2011-01-01 at the Wayback Machine [ full citation needed ]
  3. ↑ Huang, W.; Massouras, A.; Inoue, Y.; Peiffer, J.; Ramia, M.; Tarone, A. M.; Turlapati, L.; Zichner, T.; Zhu, D.; Lyman, R. F.; Magwire, M. M.; Blankenburg, K.; Carbone, M. A.; Chang, K.; Ellis, L. L.; Fernandez, S.; Han, Y.; Highnam, G.; Hjelmen, C. E.; Jack, J. R.; Javaid, M.; Jayaseelan, J.; Kalra, D.; Lee, S.; Lewis, L.; Munidasa, M.; Ongeri, F.; Patel, S.; Perales, L.; Perez, A.; Pu, L.; Rollmann, S. M.; Ruth, R.; Saada, N.; Warner, C.; Williams, A.; Wu, Y.-Q.; Yamamoto, A.; Zhang, Y.; Zhu, Y.; Anholt, R. R. H.; Korbel, J. O.; Mittelman, D.; Muzny, D. M.; Gibbs, R. A.; Barbadilla, A.; Johnston, J. S.; Stone, E. A.; Richards, S.; Deplancke, B.; Mackay, T. F. C. (8 April 2014). "Natural variation in genome architecture among 205 Drosophila melanogaster Genetic Reference Panel lines". Genome Research. 24 (7): 1193–1208. doi:10.1101/gr.171546.113. PMC   4079974 . PMID   24714809.
  4. ↑ "HGSC at Baylor College of Medicine". Archived from the original on 2010-12-19. Retrieved 2011-02-17.
  5. ↑ "Studies : Browse : Sequence Read Archive : NCBI/NLM/NIH". trace.ncbi.nlm.nih.gov.
  6. ↑ Hughes, Virginia (14 June 2010). "A wake-up call for dozing Drosophila". Nature. doi:10.1038/news.2010.298.
  7. ↑ Reed, Laura K.; Williams, Stephanie; Springston, Mastafa; Brown, Julie; Freeman, Kenda; DesRoches, Christie E.; Sokolowski, Marla B.; Gibson, Greg (July 2010). "Genotype-by-Diet Interactions Drive Metabolic Phenotype Variation in Drosophila melanogaster". Genetics. 185 (3): 1009–1019. doi:10.1534/genetics.109.113571. PMC   2907188 . PMID   20385784.
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