Genetics and Genomics

Research line n.2: Isolation of full length cDNAs in type 2 diabetes

Staff

Group leader: GIORGIO SESTI

Universita' degli Studi di ROMA "Tor Vergata"
Medicina e Chirurgia
Affiation Dipartimento di medicina Interna


1. FEDERICI MASSIMO Università di Roma Tor Vergata Dipartimento di Medicina Interna
2. SANGIUOLO FEDERICA Università di Roma Tor Vergata Dipartimento di Biopatiologia e Diagnostica Per Immagini

 

Research activity


The research line n.2 is focused to efficiently generate and isolate high quality, full-length coding sequences from information contained in Type 2 diabetes-specific expressed sequence tags (ESTs).
Generation of full-length cDNA clones is fundamental to provide accurate and complete information for gene structure and functional analysis. Most of the current approaches for mapping disease-susceptible genes are able to identify and isolate only partial expressed sequences. The common subsequent step consisting in the screening of a specific cDNA library is very tedious, laborious and often not even sufficient to obtain full-length coding sequences. In fact, despite the development of numerous strategies for constructing full-length cDNA libraries, most of these libraries contain partial cDNA clones (0.5-2 kb) lacking sequences at the 5'end. Rapid amplification of cDNA end (RACE) has been used to clone full-length cDNAs. However, production of a full-length cDNA clone by RACE requires substantial subcloning and ligation of different partial sequences. Thus, the entire process of obtaining full-length cDNA clones is still highly inefficient and time-consuming. An alternative strategy able of bypassing the library screening step can be extremely useful also in the characterization of differentially expressed genes. Methodologies that are commonly used for isolating unknown differentially expressed genes only identify short cDNA fragments that need to be fully characterized by the additional methods cited above.
The strategy proposed will use a novel library-free approach that enables rapid isolation of distinct mRNA species and subsequent production of full-length cDNA clones by a capture-primer enrichment technology (Patent pending). The principle underlying this approach has been already validated using the human actin genes as a model target cDNA (1,2).
Our analysis will start from specific type 2 diabetes ESTs that will be isolated by differential display or PCR-based subtractive hybridization strategy (3) from total cellular RNA extracted by fat and skeletal muscle biopsies obtained from subphenotypes of the first-degree relatives (FDR) of patients with Type II diabetes for the identification of specific genes that are dysregulated and associated with risk for Type 2 diabetes.
Starting from these specific expressed sequence, full length cDNAs clones will readily be cloned using this novel library-free system. The proposed method is based on the enrichment for a gene or EST-specific mRNA prior to cDNA synthesis, and as such would also insure representation of low abundance mRNA species, while in conventional cDNA libraries, these rarely expressed mRNA occur at a frequency of £ 10-6. The hypothesis that underlies this approach is that full-length cDNA are more readily synthesized with relatively homogeneous, EST-specific mRNAs than a heterogeneous population of poly(A)+ RNA. By hybridizing with EST-derived biotin labeled antisense primers, EST-specific mRNAs will be captured and isolated from total cellular RNA with streptavidin-coated magnetic beads. The enriched and purified EST-specific mRNA will then be used for an improved version of cDNA synthesis and cloned into expression plasmid vectors. Screening for desired clones would be performed by multiplex primer-specific PCR. Since the cDNA clones are derived from highly enriched mRNAs it is expected that screening for full-length cDNA clones will be more efficient and more cost-effective than it would be for screening a conventional cDNA library. Positive clones will be subjected to automatic sequencing and gene structure characterisation. They will then investigated to search causative SNPs as described in Research line 1.


References

 

1. Xu Z. and Gruenert, D.C. Development of a library-free system for EST-specific full-length cDNA cloning. Genome Tri-conference, San Francisco, CA (1998).
2. Xu Z., Jablons D.M., Gruenert D.C. EST-specific full-length cDNA clonong: actin cDNAs. submitted (2000)
3. Zhu F., Yan W., Zhao Z.L., Chai Y.B. et al. Improved PCR-based subtractive hybridization strategy for cloning differentially expressed genes. BioTechniques 29:310-313 (2000).


Financial support

 

Amount (ML) 75
Source(s) Italian Telethon and Italian Ministry of Health

 

Five recent papers


1) Hribal ML, Federici M, Porzio O, Lauro D, Borboni P, Accili D, Lauro R, Sesti G The Gly-->Arg972 amino acid polymorphism in insulin receptor substrate-1 affects glucose metabolism in skeletal muscle cells. J Clin Endocrinol Metab 2000 May;85(5):2004-13

2) Federici M, Giaccari A, Hribal ML, Giovannone B, Lauro D, Morviducci L, Pastore L, Tamburrano G, Lauro R, Sesti G Evidence for glucose/hexosamine in vivo regulation of insulin/IGF-I hybrid receptor assembly. Diabetes 1999 Dec;48(12):2277-85

3) Porzio O, Federici M, Hribal ML, Lauro D, Accili D, Lauro R, Borboni P, Sesti G. The Gly972-->Arg amino acid polymorphism in IRS-1 impairs insulin secretion in pancreatic beta cells.J Clin Invest 1999 Aug;104(3):357-64.

4) Federici M, Lauro D, D'Adamo M, Giovannone B, Porzio O, Mellozzi M, Tamburrano G, Sbraccia P, Sesti G Expression of insulin/IGF-I hybrid receptors is increased in skeletal muscle of patients with chronic primary hyperinsulinemia. Diabetes 1998 Jan;47(1):87-92

5) Federici M, Zucaro L, Porzio O, Massoud R, Borboni P, Lauro D, Sesti G Increased expression of insulin/insulin-like growth factor-I hybrid receptors in skeletal muscle of noninsulin-dependent diabetes mellitus subjects. J Clin Invest 1996 Dec 15;98(12):2887-93