Global InformationPeriannan Senapathy information
Dr. Periannan Senapathy | |
|---|---|
| Born | Namakkal, Tamil Nadu, India |
| Alma mater | Loyola College Madras University Indian Institute of Science |
| Known for | Genomics Clinical Genomics RNA Splicing Split genes |
| Scientific career | |
| Institutions | National Institutes of Health University of Wisconsin, Madison |
| Website | Genome International Corporation |
Periannan Senapathy is a molecular biologist, geneticist, author and entrepreneur. He is the founder, president and chief scientific officer at Genome International Corporation, a biotechnology, bioinformatics, and information technology firm based in Madison, Wisconsin, which develops computational genomics applications of next-generation DNA sequencing (NGS) and clinical decision support systems for analyzing patient genome data that aids in diagnosis and treatment of diseases.
Dr. Senapathy is known for his contributions in genetics, genomics and clinical genomics, especially in the biology of RNA splicing and the split structure of eukaryotic genes.[1][2][3][4][5][6][7] He developed the Shapiro & Senapathy algorithm (S&S) for predicting the splice sites, exons and genes of eukaryotes, which has become the primary methodology for discovering disease-causing mutations in splice junctions. The S&S has been implemented in many gene-finding and mutation detection tools that are used extensively in major clinical and research institutions around the world for uncovering mutations in thousands of patients with numerous diseases, including cancers and inherited disorders.[8][9][10][11][12] It is increasingly used in the Next Generation Sequencing era, as it is widely realized that >50% of all diseases and adverse drug reactions in humans and other animals possibly occur within the splicing regions of genes.[13][14][15][16][17][18][19] The S&S algorithm has been cited in ~4,000 publications on finding splicing mutations in thousands of cancer and inherited disorders.
Dr. Senapathy offered a new hypothesis on the origin of introns, split genes and splice junctions in eukaryotic genes. As the split structure of genes is central to eukaryotic biology, their origin has been a major question in biology. Dr. Senapathy proposed the "split gene theory," which states that the split structure arose due to the origin of split genes from random DNA sequences, and provided tangible evidence from genome sequences of several organisms.[1][2][4][5] He also showed that the splice junctions of eukaryotic genes could have originated from the stop codon ends of the Open Reading Frames (ORFs) in random DNA sequences based on analysis of eukaryotic genomic DNA sequences. Dr. Marshall Nirenberg, the Nobel Laureate who had deciphered codons, communicated the papers to the PNAS.[1][2] Senapathy has published his other scientific findings in journals including Science, Nucleic Acids Research, PNAS, Journal of Biological Chemistry, and Journal of Molecular Biology, and is the author of several patents in the genomics field.
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:0was invoked but never defined (see the help page). - ^ Shapiro, M. B.; Senapathy, P. (11 September 1987). "RNA splice junctions of different classes of eukaryotes: sequence statistics and functional implications in gene expression". Nucleic Acids Research. 15 (17): 7155–7174. doi:10.1093/nar/15.17.7155. ISSN 0305-1048. PMC 306199. PMID 3658675.
- ^ a b Senapathy, Periannan; Singh, Chandan Kumar; Bhasi, Ashwini; Regulapati, Rahul (20 October 2008). "Origination of the Split Structure of Spliceosomal Genes from Random Genetic Sequences". PLOS ONE. 3 (10): e3456. Bibcode:2008PLoSO...3.3456R. doi:10.1371/journal.pone.0003456. ISSN 1932-6203. PMC 2565106. PMID 18941625.
- ^ a b Senapathy, P. (2 June 1995). "Introns and the origin of protein-coding genes". Science. 268 (5215): 1366–1367. Bibcode:1995Sci...268.1366S. doi:10.1126/science.7761858. ISSN 1095-9203. PMID 7761858.
- ^ Harris, N L; Senapathy, P (25 May 1990). "Distribution and consensus of branch point signals in eukaryotic genes: a computerized statistical analysis". Nucleic Acids Research. 18 (10): 3015–3019. doi:10.1093/nar/18.10.3015. ISSN 0305-1048. PMC 330832. PMID 2349097.
- ^ Senapathy, P.; Shapiro, M. B.; Harris, N. L. (1990). [16] Splice junctions, branch point sites, and exons: Sequence statistics, identification, and applications to genome project. Methods in Enzymology. Vol. 183. pp. 252–278. doi:10.1016/0076-6879(90)83018-5. ISBN 9780121820848. ISSN 0076-6879. PMID 2314278.
- ^ Béroud, Christophe; Claustres, Mireille; Collod-Béroud, Gwenaëlle; Lalande, Marine; Hamroun, Dalil; Desmet, François-Olivier (1 May 2009). "Human Splicing Finder: an online bioinformatics tool to predict splicing signals". Nucleic Acids Research. 37 (9): e67. doi:10.1093/nar/gkp215. ISSN 0305-1048. PMC 2685110. PMID 19339519.
- ^ "Splice-Site Analyzer Tool". ibis.tau.ac.il. Retrieved 5 December 2018.
- ^ Buratti, Emanuele; Chivers, Martin; Hwang, Gyulin; Vorechovsky, Igor (January 2011). "DBASS3 and DBASS5: databases of aberrant 3'- and 5'-splice sites". Nucleic Acids Research. 39 (Database issue): D86–91. doi:10.1093/nar/gkq887. ISSN 1362-4962. PMC 3013770. PMID 20929868.
- ^ Houdayer, Claude (2011). "In Silico Prediction of Splice-Affecting Nucleotide Variants". In Silico Tools for Gene Discovery. Methods in Molecular Biology. Vol. 760. pp. 269–281. doi:10.1007/978-1-61779-176-5_17. ISBN 978-1-61779-175-8. PMID 21780003.
- ^ Schwartz, Schraga; Hall, Eitan; Ast, Gil (July 2009). "SROOGLE: webserver for integrative, user-friendly visualization of splicing signals". Nucleic Acids Research. 37 (Web Server issue): W189–192. doi:10.1093/nar/gkp320. ISSN 1362-4962. PMC 2703896. PMID 19429896.
- ^ López-Bigas, Núria; Audit, Benjamin; Ouzounis, Christos; Parra, Genís; Guigó, Roderic (28 March 2005). "Are splicing mutations the most frequent cause of hereditary disease?". FEBS Letters. 579 (9): 1900–1903. doi:10.1016/j.febslet.2005.02.047. ISSN 1873-3468. PMID 15792793.
- ^ Estivill, Xavier; Lázaro, Conxi; Gaona, Antonia; Kruyer, Helena; García, Judit; Serra, Eduard; Ars, Elisabet (22 January 2000). "Mutations affecting mRNA splicing are the most common molecular defects in patients with neurofibromatosis type 1". Human Molecular Genetics. 9 (2): 237–247. doi:10.1093/hmg/9.2.237. ISSN 0964-6906. PMID 10607834.
- ^ Concannon, Patrick; Gatti, Richard A.; Bernatowska, Eva; Sanal, Özden; Chessa, Luciana; Tolun, Asli; Önengüt, Suna; Liang, Teresa; Becker-Catania, Sara (1 June 1999). "Splicing Defects in the Ataxia-Telangiectasia Gene, ATM: Underlying Mutations and Consequences". The American Journal of Human Genetics. 64 (6): 1617–1631. doi:10.1086/302418. ISSN 1537-6605. PMC 1377904. PMID 10330348.
- ^ Lázaro, C.; Estivill, X.; Ravella, A.; Serra, E.; Pros, E.; Morell, M.; Kruyer, H.; Ars, E. (1 June 2003). "Recurrent mutations in the NF1 gene are common among neurofibromatosis type 1 patients". Journal of Medical Genetics. 40 (6): e82. doi:10.1136/jmg.40.6.e82. ISSN 1468-6244. PMC 1735494. PMID 12807981.
- ^ Bozon, Dominique; Rousson, Robert; Rouvet, Isabelle; Bonnet, Véronique; Albuisson, Juliette; Millat, Gilles; Crehalet, Hervé (5 June 2012). "Combined use of in silico and in vitro splicing assays for interpretation of genomic variants of unknown significance in cardiomyopathies and channelopathies". Cardiogenetics. 2 (1): e6. doi:10.4081/cardiogenetics.2012.e6. ISSN 2035-8148.
- ^ Schmutzler, Rita K.; Meindl, Alfons; Hahnen, Eric; Rhiem, Kerstin; Arnold, Norbert; Kast, Karin; Köhler, Juliane; Engert, Stefanie; Weber, Ute (11 December 2012). "Analysis of 30 Putative BRCA1 Splicing Mutations in Hereditary Breast and Ovarian Cancer Families Identifies Exonic Splice Site Mutations That Escape In Silico Prediction". PLOS ONE. 7 (12): e50800. Bibcode:2012PLoSO...750800W. doi:10.1371/journal.pone.0050800. ISSN 1932-6203. PMC 3519833. PMID 23239986.
- ^ Barta, Andrea; Schumperli, Daniel (2010). "Editorial on alternative splicing and disease". RNA Biology. 7 (4): 388–389. doi:10.4161/rna.7.4.12818. PMID 21140604.