COLLEGE OF MEDICINE AND HEALTH
Medicine, Nursing and Allied Health Professions

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 Jonathan Locke

Jonathan Locke

Postgraduate Research Associate / Associate Lecturer

 01392 408205

 RILD Building Level 3

 

University of Exeter Medical School, RILD Building, RD&E Hospital Wonford, Barrack Road, Exeter, EX2 5DW, UK

Overview

Dr Locke received a Masters of Biology in Molecular & Cellular Biology from the University of Bath in 2006. Following this he obtained a PhD from the Peninsula Medical School (Universities of Exeter & Plymouth) under the supervision of Dr Lorna Harries. During his doctoral studies he became interested in understanding how the non-protein coding genome impacts upon common and rare forms of diabetes mellitus.  Following completion of his PhD he has continued to work in this area with papers published on the role of miRNAs in diabetes and changes in protein-coding expression in mediating susceptibility to diabetes.  His current interests revolve around using accessible human tissue to understand molecular mechanisms in diabetes.

Dr Locke also teaches on the MSc Genomic Medicine and BSc Medical Sciences programmes. He is, in particular, interested in developing student’s transferable skills, developing such material for Academic Tutor Groups and taught modules (e.g. Professional & Research Skills).

Qualifications

  • PhD (Medical Studies), Peninsula Medical School, Universities of Exeter & Plymouth
  • Master of Biology (MBiol) Molecular & Cellular Biology, University of Bath

Research

Research interests

Dr Locke is interested in elucidating the role of the non-protein coding genome in diabetes susceptibility.

Research projects

Current Projects:

  • Using minimally-invasive human tissue (e.g. blood, urine) to aid in the genetic diagnosis of monogenic diabetes.

Grants/Funding:

  • Northcott Devon Medical Foundation (£5100) for grant entitled ‘Using patient accessible tissues to aid the genetic diagnosis of MODY and deliver personalised medicine’.

 

 

Publications

Key publications | Publications by category | Publications by year

Publications by category


Journal articles

Locke JM, da Silva Xavier G, Rutter, GA, Harries LW (In Press). An alternative polyadenylation signal in TCF7L2 generates isoforms that inhibit T cell factor/lymphoid-enhancer factor (TCF/LEF)-dependent target genes. Diabetologia Abstract.  Full text.
Lee BP, Lloyd-Laney HO, Locke JM, McCulloch LJ, Knight B, Yaghootkar H, Cory G, Kos K, Frayling TM, Harries LW, et al (In Press). Functional characterisation of ADIPOQ variants using individuals recruited by genotype. Mol Cell Endocrinol, 428, 49-57. Abstract.  Author URL.  Full text.
Locke JM, Saint-Martin C, Laver TW, Patel KA, Wood AR, Sharp SA, Ellard S, Bellanné-Chantelot C, Hattersley AT, Harries LW, et al (In Press). The Common HNF1A Variant I27L is a Modifier of Age at Diabetes Diagnosis in Individuals with HNF1A-MODY. Diabetes, 67(9), 1903-1907. Abstract.  Author URL.  Full text.
Frayling TM (2018). A Common Allele in FGF21 Associated with Sugar Intake is Associated with Body Shape, Lower Total Body-Fat Percentage, and Higher Blood Pressure. Cell Reports, 23(2), 327-336. Full text.
Tugay K, Guay C, Marques AC, Allagnat F, Locke JM, Harries LW, Rutter GA, Regazzi R (2016). Role of microRNAs in the age-associated decline of pancreatic beta cell function in rat islets. Diabetologia, 59(1), 161-169. Abstract.
Locke JM, Wei FY, Tomizawa K, Weedon MN, Harries LW (2015). A cautionary tale: the non-causal association between type 2 diabetes risk SNP, rs7756992, and levels of non-coding RNA, CDKAL1-v1. Diabetologia, 58(4), 745-748. Abstract.  Full text.
Locke JM, Hysenaj G, Wood AR, Weedon MN, Harries LW (2015). Targeted allelic expression profiling in human islets identifies cis-regulatory effects for multiple variants identified by type 2 diabetes genome-wide association studies. Diabetes, 64(4), 1484-1491. Abstract.  Author URL.  Full text.
Locke JM, Lango Allen H, Harries LW (2014). A rare SNP in pre-miR-34a is associated with increased levels of miR-34a in pancreatic beta cells. Acta Diabetologica, 51(2), 325-329. Abstract.  Full text.
Locke JM, Da Silva Xavier G, Dawe HR, Rutter GA, Harries LW (2014). Increased expression of miR-187 in human islets from individuals with type 2 diabetes is associated with reduced glucose-stimulated insulin secretion. Diabetologia, 57(1), 122-128. Abstract.  Full text.
Morrison F, Locke J, Arif M, Murray A, Brown JE, Harries LW (2013). Expression profiling of type 2 diabetes susceptibility genes in the pancreatic islets, adipose tissue and liver of obese mice. Exp Clin Endocrinol Diabetes, 121(7), 413-419. Abstract.  Author URL.
Morrison FS, Locke JM, Wood AR, Tuke M, Pasko D, Murray A, Frayling T, Harries LW (2013). The splice site variant rs11078928 may be associated with a genotype-dependent alteration in expression of GSDMB transcripts. BMC Genomics, 14 Abstract.  Author URL.  Full text.
Locke JM, Harries LW (2012). MicroRNA expression profiling of human islets from individuals with and without type 2 diabetes: promises and pitfalls. Biochem Soc Trans, 40(4), 800-803. Abstract.  Author URL.
Morrison F, Johnstone K, Murray A, Locke J, Harries LW (2012). Oxidative metabolism genes are not responsive to oxidative stress in rodent beta cell lines. Experimental Diabetes Research, 2012 Abstract.  Full text.
Flanagan SE, Patch A-M, Locke JM, Akcay T, Simsek E, Alaei M, Yekta Z, Desai M, Kapoor RR, Hussain K, et al (2011). Genome-wide homozygosity analysis reveals HADH mutations as a common cause of diazoxide-responsive hyperinsulinemic-hypoglycemia in consanguineous pedigrees. J Clin Endocrinol Metab, 96(3), E498-E502. Abstract.  Author URL.
Garin I, Edghill EL, Akerman I, Rubio-Cabezas O, Rica I, Locke JM, Maestro MA, Alshaikh A, Bundak R, Del Castillo G, et al (2010). Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis. Proceedings of the National Academy of Sciences of the United States of America, 107(7), 3105-3110. Abstract.
Locke JM, Ellard S, Norwood VF, Harries LW (2009). Variants in the isoform-specific coding regions of the HNF1A, HNF4A and HNF1B genes are not a common cause of familial, young-onset diabetes or renal cysts and diabetes (RCAD). DIABETIC MEDICINE, 26(5), 570-570. Author URL.
Kapoor RR, Locke J, Colclough K, Wales J, Conn JJ, Hattersley AT, Ellard S, Hussain K (2008). Persistent hyperinsulinemic hypoglycemia and maturity-onset diabetes of the young due to heterozygous HNF4A mutations. Diabetes, 57(6), 1659-1663. Abstract.  Author URL.
Locke JM, Harries LW (2008). RNA processing and mRNA surveillance in monogenic diabetes. Gene Regul Syst Bio, 2, 203-212. Abstract.  Author URL.  Full text.
Harries LW, Locke JM, Shields B, Hanley NA, Hanley KP, Steele A, Njølstad PR, Ellard S, Hattersley AT (2008). The diabetic phenotype in HNF4A mutation carriers is moderated by the expression of HNF4A isoforms from the P1 promoter during fetal development. Diabetes, 57(6), 1745-1752. Abstract.  Author URL.

Conferences

Locke JM, Patel KA, Shepherd MH, Ellard S, Weedon MN (2018). Expression of Maturity-Onset Diabetes of the Young (MODY) genes in accessible human tissues.  Author URL.

Publications by year


In Press

Locke JM, da Silva Xavier G, Rutter, GA, Harries LW (In Press). An alternative polyadenylation signal in TCF7L2 generates isoforms that inhibit T cell factor/lymphoid-enhancer factor (TCF/LEF)-dependent target genes. Diabetologia Abstract.  Full text.
Lee BP, Lloyd-Laney HO, Locke JM, McCulloch LJ, Knight B, Yaghootkar H, Cory G, Kos K, Frayling TM, Harries LW, et al (In Press). Functional characterisation of ADIPOQ variants using individuals recruited by genotype. Mol Cell Endocrinol, 428, 49-57. Abstract.  Author URL.  Full text.
Locke JM, Saint-Martin C, Laver TW, Patel KA, Wood AR, Sharp SA, Ellard S, Bellanné-Chantelot C, Hattersley AT, Harries LW, et al (In Press). The Common HNF1A Variant I27L is a Modifier of Age at Diabetes Diagnosis in Individuals with HNF1A-MODY. Diabetes, 67(9), 1903-1907. Abstract.  Author URL.  Full text.

2018

Frayling TM (2018). A Common Allele in FGF21 Associated with Sugar Intake is Associated with Body Shape, Lower Total Body-Fat Percentage, and Higher Blood Pressure. Cell Reports, 23(2), 327-336. Full text.
Locke JM, Patel KA, Shepherd MH, Ellard S, Weedon MN (2018). Expression of Maturity-Onset Diabetes of the Young (MODY) genes in accessible human tissues.  Author URL.

2016

Tugay K, Guay C, Marques AC, Allagnat F, Locke JM, Harries LW, Rutter GA, Regazzi R (2016). Role of microRNAs in the age-associated decline of pancreatic beta cell function in rat islets. Diabetologia, 59(1), 161-169. Abstract.

2015

Locke JM, Wei FY, Tomizawa K, Weedon MN, Harries LW (2015). A cautionary tale: the non-causal association between type 2 diabetes risk SNP, rs7756992, and levels of non-coding RNA, CDKAL1-v1. Diabetologia, 58(4), 745-748. Abstract.  Full text.
Locke JM, Hysenaj G, Wood AR, Weedon MN, Harries LW (2015). Targeted allelic expression profiling in human islets identifies cis-regulatory effects for multiple variants identified by type 2 diabetes genome-wide association studies. Diabetes, 64(4), 1484-1491. Abstract.  Author URL.  Full text.

2014

Locke JM, Lango Allen H, Harries LW (2014). A rare SNP in pre-miR-34a is associated with increased levels of miR-34a in pancreatic beta cells. Acta Diabetologica, 51(2), 325-329. Abstract.  Full text.
Locke JM, Da Silva Xavier G, Dawe HR, Rutter GA, Harries LW (2014). Increased expression of miR-187 in human islets from individuals with type 2 diabetes is associated with reduced glucose-stimulated insulin secretion. Diabetologia, 57(1), 122-128. Abstract.  Full text.

2013

Morrison F, Locke J, Arif M, Murray A, Brown JE, Harries LW (2013). Expression profiling of type 2 diabetes susceptibility genes in the pancreatic islets, adipose tissue and liver of obese mice. Exp Clin Endocrinol Diabetes, 121(7), 413-419. Abstract.  Author URL.
Morrison FS, Locke JM, Wood AR, Tuke M, Pasko D, Murray A, Frayling T, Harries LW (2013). The splice site variant rs11078928 may be associated with a genotype-dependent alteration in expression of GSDMB transcripts. BMC Genomics, 14 Abstract.  Author URL.  Full text.

2012

Locke JM, Harries LW (2012). MicroRNA expression profiling of human islets from individuals with and without type 2 diabetes: promises and pitfalls. Biochem Soc Trans, 40(4), 800-803. Abstract.  Author URL.
Morrison F, Johnstone K, Murray A, Locke J, Harries LW (2012). Oxidative metabolism genes are not responsive to oxidative stress in rodent beta cell lines. Experimental Diabetes Research, 2012 Abstract.  Full text.

2011

Flanagan SE, Patch A-M, Locke JM, Akcay T, Simsek E, Alaei M, Yekta Z, Desai M, Kapoor RR, Hussain K, et al (2011). Genome-wide homozygosity analysis reveals HADH mutations as a common cause of diazoxide-responsive hyperinsulinemic-hypoglycemia in consanguineous pedigrees. J Clin Endocrinol Metab, 96(3), E498-E502. Abstract.  Author URL.

2010

Garin I, Edghill EL, Akerman I, Rubio-Cabezas O, Rica I, Locke JM, Maestro MA, Alshaikh A, Bundak R, Del Castillo G, et al (2010). Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis. Proceedings of the National Academy of Sciences of the United States of America, 107(7), 3105-3110. Abstract.

2009

Locke JM, Ellard S, Norwood VF, Harries LW (2009). Variants in the isoform-specific coding regions of the HNF1A, HNF4A and HNF1B genes are not a common cause of familial, young-onset diabetes or renal cysts and diabetes (RCAD). DIABETIC MEDICINE, 26(5), 570-570. Author URL.

2008

Kapoor RR, Locke J, Colclough K, Wales J, Conn JJ, Hattersley AT, Ellard S, Hussain K (2008). Persistent hyperinsulinemic hypoglycemia and maturity-onset diabetes of the young due to heterozygous HNF4A mutations. Diabetes, 57(6), 1659-1663. Abstract.  Author URL.
Locke JM, Harries LW (2008). RNA processing and mRNA surveillance in monogenic diabetes. Gene Regul Syst Bio, 2, 203-212. Abstract.  Author URL.  Full text.
Harries LW, Locke JM, Shields B, Hanley NA, Hanley KP, Steele A, Njølstad PR, Ellard S, Hattersley AT (2008). The diabetic phenotype in HNF4A mutation carriers is moderated by the expression of HNF4A isoforms from the P1 promoter during fetal development. Diabetes, 57(6), 1745-1752. Abstract.  Author URL.

Jonathan_Locke Details from cache as at 2018-12-13 20:21:24

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Teaching

Teaching responsibilities: (Undergraduate, Postgraduate)

  • Module Lead for Professional & Research Skills module on MSc Genomic Medicine
  • Facilitator on BMedSci modules: Principles of Medical Research, Medical Genomics
  • Academic Tutor on MSc Genomic Medicine and BMedSci programmes

Modules

2018/19


Supervision / Group

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