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Ireena Dutta

Dr Ireena Dutta

Interim Director
Programme and Strategy

The Programme and Strategy team is led by the Interim Director, Dr Ireena Dutta. Ireena has a PhD in antimicrobial resistance from the University of Cambridge, and extensive experience in knowledge transfer, science communication, and strategy development. She remains an enthusiastic microbiologist.

My publications

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  • Selected
  • 2005
  • 2004
  • 2003
  • 2002

Knowledge sharing and 'genomic' healthcare.

Dutta I; Brice PC; Wallace S

Nature Biotechnology 2005;23;2;169-70

The DNA sequence of the human X chromosome.

Ross MT; Grafham DV; Coffey AJ; Scherer S; McLay K; Muzny D; Platzer M; Howell GR; Burrows C; Bird CP; Frankish A; Lovell FL; Howe KL; Ashurst JL; Fulton RS; Sudbrak R; Wen G; Jones MC; Hurles ME; Andrews TD; Scott CE; Searle S; Ramser J; Whittaker A; Deadman R; Carter NP; Hunt SE; Chen R; Cree A; Gunaratne P; Havlak P; Hodgson A; Metzker ML; Richards S; Scott G; Steffen D; Sodergren E; Wheeler DA; Worley KC; Ainscough R; Ambrose KD; Ansari-Lari MA; Aradhya S; Ashwell RI; Babbage AK; Bagguley CL; Ballabio A; Banerjee R; Barker GE; Barlow KF; Barrett IP; Bates KN; Beare DM; Beasley H; Beasley O; Beck A; Bethel G; Blechschmidt K; Brady N; Bray-Allen S; Bridgeman AM; Brown AJ; Brown MJ; Bonnin D; Bruford EA; Buhay C; Burch P; Burford D; Burgess J; Burrill W; Burton J; Bye JM; Carder C; Carrel L; Chako J; Chapman JC; Chavez D; Chen E; Chen G; Chen Y; Chen Z; Chinault C; Ciccodicola A; Clark SY; Clarke G; Clee CM; Clegg S; Clerc-Blankenburg K; Clifford K; Cobley V; Cole CG; Conquer JS; Corby N; Connor RE; David R; Davies J; Davis C; Davis J; Delgado O; Deshazo D; Dhami P; Ding Y; Dinh H; Dodsworth S; Draper H; Dugan-Rocha S; Dunham A; Dunn M; Durbin KJ; Dutta I; Eades T; Ellwood M; Emery-Cohen A; Errington H; Evans KL; Faulkner L; Francis F; Frankland J; Fraser AE; Galgoczy P; Gilbert J; Gill R; Glöckner G; Gregory SG; Gribble S; Griffiths C; Grocock R; Gu Y; Gwilliam R; Hamilton C; Hart EA; Hawes A; Heath PD; Heitmann K; Hennig S; Hernandez J; Hinzmann B; Ho S; Hoffs M; Howden PJ; Huckle EJ; Hume J; Hunt PJ; Hunt AR; Isherwood J; Jacob L; Johnson D; Jones S; de Jong PJ; Joseph SS; Keenan S; Kelly S; Kershaw JK; Khan Z; Kioschis P; Klages S; Knights AJ; Kosiura A; Kovar-Smith C; Laird GK; Langford C; Lawlor S; Leversha M; Lewis L; Liu W; Lloyd C; Lloyd DM; Loulseged H; Loveland JE; Lovell JD; Lozado R; Lu J; Lyne R; Ma J; Maheshwari M; Matthews LH; McDowall J; McLaren S; McMurray A; Meidl P; Meitinger T; Milne S; Miner G; Mistry SL; Morgan M; Morris S; Müller I; Mullikin JC; Nguyen N; Nordsiek G; Nyakatura G; O'Dell CN; Okwuonu G; Palmer S; Pandian R; Parker D; Parrish J; Pasternak S; Patel D; Pearce AV; Pearson DM; Pelan SE; Perez L; Porter KM; Ramsey Y; Reichwald K; Rhodes S; Ridler KA; Schlessinger D; Schueler MG; Sehra HK; Shaw-Smith C; Shen H; Sheridan EM; Shownkeen R; Skuce CD; Smith ML; Sotheran EC; Steingruber HE; Steward CA; Storey R; Swann RM; Swarbreck D; Tabor PE; Taudien S; Taylor T; Teague B; Thomas K; Thorpe A; Timms K; Tracey A; Trevanion S; Tromans AC; d'Urso M; Verduzco D; Villasana D; Waldron L; Wall M; Wang Q; Warren J; Warry GL; Wei X; West A; Whitehead SL; Whiteley MN; Wilkinson JE; Willey DL; Williams G; Williams L; Williamson A; Williamson H; Wilming L; Woodmansey RL; Wray PW; Yen J; Zhang J; Zhou J; Zoghbi H; Zorilla S; Buck D; Reinhardt R; Poustka A; Rosenthal A; Lehrach H; Meindl A; Minx PJ; Hillier LW; Willard HF; Wilson RK; Waterston RH; Rice CM; Vaudin M; Coulson A; Nelson DL; Weinstock G; Sulston JE; Durbin R; Hubbard T; Gibbs RA; Beck S; Rogers J; Bentley DR

Nature 2005;434;7031;325-37

The human X chromosome has a unique biology that was shaped by its evolution as the sex chromosome shared by males and females. We have determined 99.3% of the euchromatic sequence of the X chromosome. Our analysis illustrates the autosomal origin of the mammalian sex chromosomes, the stepwise process that led to the progressive loss of recombination between X and Y, and the extent of subsequent degradation of the Y chromosome. LINE1 repeat elements cover one-third of the X chromosome, with a distribution that is consistent with their proposed role as way stations in the process of X-chromosome inactivation. We found 1,098 genes in the sequence, of which 99 encode proteins expressed in testis and in various tumour types. A disproportionately high number of mendelian diseases are documented for the X chromosome. Of this number, 168 have been explained by mutations in 113 X-linked genes, which in many cases were characterized with the aid of the DNA sequence.

DNA sequence and analysis of human chromosome 9.

Humphray SJ; Oliver K; Hunt AR; Plumb RW; Loveland JE; Howe KL; Andrews TD; Searle S; Hunt SE; Scott CE; Jones MC; Ainscough R; Almeida JP; Ambrose KD; Ashwell RI; Babbage AK; Babbage S; Bagguley CL; Bailey J; Banerjee R; Barker DJ; Barlow KF; Bates K; Beasley H; Beasley O; Bird CP; Bray-Allen S; Brown AJ; Brown JY; Burford D; Burrill W; Burton J; Carder C; Carter NP; Chapman JC; Chen Y; Clarke G; Clark SY; Clee CM; Clegg S; Collier RE; Corby N; Crosier M; Cummings AT; Davies J; Dhami P; Dunn M; Dutta I; Dyer LW; Earthrowl ME; Faulkner L; Fleming CJ; Frankish A; Frankland JA; French L; Fricker DG; Garner P; Garnett J; Ghori J; Gilbert JG; Glison C; Grafham DV; Gribble S; Griffiths C; Griffiths-Jones S; Grocock R; Guy J; Hall RE; Hammond S; Harley JL; Harrison ES; Hart EA; Heath PD; Henderson CD; Hopkins BL; Howard PJ; Howden PJ; Huckle E; Johnson C; Johnson D; Joy AA; Kay M; Keenan S; Kershaw JK; Kimberley AM; King A; Knights A; Laird GK; Langford C; Lawlor S; Leongamornlert DA; Leversha M; Lloyd C; Lloyd DM; Lovell J; Martin S; Mashreghi-Mohammadi M; Matthews L; McLaren S; McLay KE; McMurray A; Milne S; Nickerson T; Nisbett J; Nordsiek G; Pearce AV; Peck AI; Porter KM; Pandian R; Pelan S; Phillimore B; Povey S; Ramsey Y; Rand V; Scharfe M; Sehra HK; Shownkeen R; Sims SK; Skuce CD; Smith M; Steward CA; Swarbreck D; Sycamore N; Tester J; Thorpe A; Tracey A; Tromans A; Thomas DW; Wall M; Wallis JM; West AP; Whitehead SL; Willey DL; Williams SA; Wilming L; Wray PW; Young L; Ashurst JL; Coulson A; Blöcker H; Durbin R; Sulston JE; Hubbard T; Jackson MJ; Bentley DR; Beck S; Rogers J; Dunham I

Nature 2004;429;6990;369-74

Chromosome 9 is highly structurally polymorphic. It contains the largest autosomal block of heterochromatin, which is heteromorphic in 6-8% of humans, whereas pericentric inversions occur in more than 1% of the population. The finished euchromatic sequence of chromosome 9 comprises 109,044,351 base pairs and represents >99.6% of the region. Analysis of the sequence reveals many intra- and interchromosomal duplications, including segmental duplications adjacent to both the centromere and the large heterochromatic block. We have annotated 1,149 genes, including genes implicated in male-to-female sex reversal, cancer and neurodegenerative disease, and 426 pseudogenes. The chromosome contains the largest interferon gene cluster in the human genome. There is also a region of exceptionally high gene and G + C content including genes paralogous to those in the major histocompatibility complex. We have also detected recently duplicated genes that exhibit different rates of sequence divergence, presumably reflecting natural selection.

The DNA sequence and comparative analysis of human chromosome 10.

Deloukas P; Earthrowl ME; Grafham DV; Rubenfield M; French L; Steward CA; Sims SK; Jones MC; Searle S; Scott C; Howe K; Hunt SE; Andrews TD; Gilbert JG; Swarbreck D; Ashurst JL; Taylor A; Battles J; Bird CP; Ainscough R; Almeida JP; Ashwell RI; Ambrose KD; Babbage AK; Bagguley CL; Bailey J; Banerjee R; Bates K; Beasley H; Bray-Allen S; Brown AJ; Brown JY; Burford DC; Burrill W; Burton J; Cahill P; Camire D; Carter NP; Chapman JC; Clark SY; Clarke G; Clee CM; Clegg S; Corby N; Coulson A; Dhami P; Dutta I; Dunn M; Faulkner L; Frankish A; Frankland JA; Garner P; Garnett J; Gribble S; Griffiths C; Grocock R; Gustafson E; Hammond S; Harley JL; Hart E; Heath PD; Ho TP; Hopkins B; Horne J; Howden PJ; Huckle E; Hynds C; Johnson C; Johnson D; Kana A; Kay M; Kimberley AM; Kershaw JK; Kokkinaki M; Laird GK; Lawlor S; Lee HM; Leongamornlert DA; Laird G; Lloyd C; Lloyd DM; Loveland J; Lovell J; McLaren S; McLay KE; McMurray A; Mashreghi-Mohammadi M; Matthews L; Milne S; Nickerson T; Nguyen M; Overton-Larty E; Palmer SA; Pearce AV; Peck AI; Pelan S; Phillimore B; Porter K; Rice CM; Rogosin A; Ross MT; Sarafidou T; Sehra HK; Shownkeen R; Skuce CD; Smith M; Standring L; Sycamore N; Tester J; Thorpe A; Torcasso W; Tracey A; Tromans A; Tsolas J; Wall M; Walsh J; Wang H; Weinstock K; West AP; Willey DL; Whitehead SL; Wilming L; Wray PW; Young L; Chen Y; Lovering RC; Moschonas NK; Siebert R; Fechtel K; Bentley D; Durbin R; Hubbard T; Doucette-Stamm L; Beck S; Smith DR; Rogers J

Nature 2004;429;6990;375-81

The finished sequence of human chromosome 10 comprises a total of 131,666,441 base pairs. It represents 99.4% of the euchromatic DNA and includes one megabase of heterochromatic sequence within the pericentromeric region of the short and long arm of the chromosome. Sequence annotation revealed 1,357 genes, of which 816 are protein coding, and 430 are pseudogenes. We observed widespread occurrence of overlapping coding genes (either strand) and identified 67 antisense transcripts. Our analysis suggests that both inter- and intrachromosomal segmental duplications have impacted on the gene count on chromosome 10. Multispecies comparative analysis indicated that we can readily annotate the protein-coding genes with current resources. We estimate that over 95% of all coding exons were identified in this study. Assessment of single base changes between the human chromosome 10 and chimpanzee sequence revealed nonsense mutations in only 21 coding genes with respect to the human sequence.

The vanC-3 vancomycin resistance gene cluster of Enterococcus flavescens CCM 439.

Dutta I; Reynolds PE

The Journal of antimicrobial chemotherapy 2003;51;3;703-6

Enterococcus flavescens CCM 439 is phenotypically similar to Enterococcus casseliflavus; it possesses intrinsic low-level resistance to vancomycin and has the VanC phenotype. The complete vanC-3 vancomycin resistance gene cluster was cloned and sequenced, and found to contain five open reading frames. These encoded five proteins that displayed a high degree of amino acid identity to the proteins of the vanC-2 cluster of E. casseliflavus. The serine racemases displayed the lowest degree of identity (97%), whereas the response regulators VanR(C-2) and VanR(C-3) were 100% identical. Long-PCR-RFLP analysis of the vanC-3 and vanC-2 gene clusters distinguished E. flavescens CCM 439 from E. casseliflavus ATCC 25788 due to the absence of a single EcoRV restriction endonuclease site from the E. flavescens gene cluster. However, the lack of nucleotide divergence between the sequences of the vanC-2 and vanC-3 clusters casts doubt on the validity of E. flavescens and E. casseliflavus being classed as distinct species.

Biochemical and genetic characterization of the vanC-2 vancomycin resistance gene cluster of Enterococcus casseliflavus ATCC 25788.

Dutta I; Reynolds PE

Antimicrobial agents and chemotherapy 2002;46;10;3125-32

The vanC-2 cluster of Enterococcus casseliflavus ATCC 25788 consisted of five genes (vanC-2, vanXY(C-2), vanT(C-2), vanR(C-2), and vanS(C-2)) and shared the same organization as the vanC cluster of E. gallinarum BM4174. The proteins encoded by these genes displayed a high degree of amino acid identity to the proteins encoded within the vanC gene cluster. The putative D,D-dipeptidase-D,D-carboxypeptidase, VanXY(C-2), exhibited 81% amino acid identity to VanXY(C), and VanT(C-2) displayed 65% amino acid identity to the serine racemase, VanT. VanR(C-2) and VanS(C-2) displayed high degrees of identity to VanR(C) and VanS(C), respectively, and contained the conserved residues identified as important to their function as a response regulator and histidine kinase, respectively. Resistance to vancomycin was expressed inducibly in E. casseliflavus ATCC 25788 and required an extended period of induction. Analysis of peptidoglycan precursors revealed that UDP-N-acetylmuramyl-L-Ala-delta-D-Glu-L-Lys-D-Ala-D-Ser could not be detected until several hours after the addition of vancomycin, and its appearance coincided with the resumption of growth. The introduction of additional copies of the vanT(C-2) gene, encoding a putative serine racemase, and the presence of supplementary D-serine in the growth medium both significantly reduced the period before growth resumed after addition of vancomycin. This suggested that the availability of D-serine plays an important role in the induction process.