Gamble JA

References (2)

Title : Comparative genomics of the fungal pathogens Candida dubliniensis and Candida albicans - Jackson_2009_Genome.Res_19_2231
Author(s) : Jackson AP , Gamble JA , Yeomans T , Moran GP , Saunders D , Harris D , Aslett M , Barrell JF , Butler G , Citiulo F , Coleman DC , de Groot PW , Goodwin TJ , Quail MA , McQuillan J , Munro CA , Pain A , Poulter RT , Rajandream MA , Renauld H , Spiering MJ , Tivey A , Gow NA , Barrell B , Sullivan DJ , Berriman M
Ref : Genome Res , 19 :2231 , 2009
Abstract : Candida dubliniensis is the closest known relative of Candida albicans, the most pathogenic yeast species in humans. However, despite both species sharing many phenotypic characteristics, including the ability to form true hyphae, C. dubliniensis is a significantly less virulent and less versatile pathogen. Therefore, to identify C. albicans-specific genes that may be responsible for an increased capacity to cause disease, we have sequenced the C. dubliniensis genome and compared it with the known C. albicans genome sequence. Although the two genome sequences are highly similar and synteny is conserved throughout, 168 species-specific genes are identified, including some encoding known hyphal-specific virulence factors, such as the aspartyl proteinases Sap4 and Sap5 and the proposed invasin Als3. Among the 115 pseudogenes confirmed in C. dubliniensis are orthologs of several filamentous growth regulator (FGR) genes that also have suspected roles in pathogenesis. However, the principal differences in genomic repertoire concern expansion of the TLO gene family of putative transcription factors and the IFA family of putative transmembrane proteins in C. albicans, which represent novel candidate virulence-associated factors. The results suggest that the recent evolutionary histories of C. albicans and C. dubliniensis are quite different. While gene families instrumental in pathogenesis have been elaborated in C. albicans, C. dubliniensis has lost genomic capacity and key pathogenic functions. This could explain why C. albicans is a more potent pathogen in humans than C. dubliniensis.
ESTHER : Jackson_2009_Genome.Res_19_2231
PubMedSearch : Jackson_2009_Genome.Res_19_2231
PubMedID: 19745113
Gene_locus related to this paper: canal-ATG15 , canal-c4yl13 , canal-ppme1 , canal-q5a0c9 , canal-q5ad17 , canal-q5ady2 , canal-q5ag57 , canal-q5ai12 , canal-q5akz5 , canal-q5apu4 , canal-q59m48 , canal-q59nw6 , candc-b9w8x6 , candc-b9w8x7 , candc-b9w905 , candc-b9wa64 , candc-b9wc27 , candc-b9wc30 , candc-b9wc93 , candc-b9wce3 , candc-b9wdh9 , candc-b9wds3 , candc-b9whs3 , candc-b9whs6 , candc-b9whv2 , candc-b9wi60 , candc-b9wid3 , candc-b9wje5 , candc-b9wk97 , candc-CduLAc , candc-b9wkf5 , candc-b9wkj1 , candc-b9wlf0 , candc-b9wmt8 , candc-b9wmx4 , candc-b9wc51 , candc-b9wa43 , candc-b9wl19 , candc-kex1

Title : The genome of the blood fluke Schistosoma mansoni - Berriman_2009_Nature_460_352
Author(s) : Berriman M , Haas BJ , LoVerde PT , Wilson RA , Dillon GP , Cerqueira GC , Mashiyama ST , Al-Lazikani B , Andrade LF , Ashton PD , Aslett MA , Bartholomeu DC , Blandin G , Caffrey CR , Coghlan A , Coulson R , Day TA , Delcher A , DeMarco R , Djikeng A , Eyre T , Gamble JA , Ghedin E , Gu Y , Hertz-Fowler C , Hirai H , Hirai Y , Houston R , Ivens A , Johnston DA , Lacerda D , Macedo CD , McVeigh P , Ning Z , Oliveira G , Overington JP , Parkhill J , Pertea M , Pierce RJ , Protasio AV , Quail MA , Rajandream MA , Rogers J , Sajid M , Salzberg SL , Stanke M , Tivey AR , White O , Williams DL , Wortman J , Wu W , Zamanian M , Zerlotini A , Fraser-Liggett CM , Barrell BG , El-Sayed NM
Ref : Nature , 460 :352 , 2009
Abstract : Schistosoma mansoni is responsible for the neglected tropical disease schistosomiasis that affects 210 million people in 76 countries. Here we present analysis of the 363 megabase nuclear genome of the blood fluke. It encodes at least 11,809 genes, with an unusual intron size distribution, and new families of micro-exon genes that undergo frequent alternative splicing. As the first sequenced flatworm, and a representative of the Lophotrochozoa, it offers insights into early events in the evolution of the animals, including the development of a body pattern with bilateral symmetry, and the development of tissues into organs. Our analysis has been informed by the need to find new drug targets. The deficits in lipid metabolism that make schistosomes dependent on the host are revealed, and the identification of membrane receptors, ion channels and more than 300 proteases provide new insights into the biology of the life cycle and new targets. Bioinformatics approaches have identified metabolic chokepoints, and a chemogenomic screen has pinpointed schistosome proteins for which existing drugs may be active. The information generated provides an invaluable resource for the research community to develop much needed new control tools for the treatment and eradication of this important and neglected disease.
ESTHER : Berriman_2009_Nature_460_352
PubMedSearch : Berriman_2009_Nature_460_352
PubMedID: 19606141
Gene_locus related to this paper: schma-ACHE1 , schma-ACHE2 , schma-c4qb79 , schma-c4qmk4 , schma-g4v9h7 , schma-BCHE , schma-g4vmf3