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Table of contents
I. Chlamydia trachomatis, a human-adapted obligate intracellular pathogen
A. C. trachomatis phylogeny and associated pathologies
B. A bacterium with a peculiar biphasic developmental cycle
C. Host-bacterium interactions
II. Glucose metabolism during Chlamydia infection
A. Glucose in mammalian cells, an energy source and a biosynthesis precursor
B. C. trachomatis and glucose: a long story
C. Glucose metabolism modifications in Chlamydia-infected cell
III. The Tissue Transglutaminase, a cellular enzyme
A. TG2, a member of the transglutaminase family
B. Regulation of TG2 transglutaminase activity
C. Physiopathological importance of TG2
IV. Questions addressed in this doctoral work
I. TG2 is expressed at high level and activated during C. trachomatis infection
II. TG2 activity sustains bacterial growth
A. In cellulo
B. In vivo
III. TG2 plays a central role in metabolic rewiring during infection
IV. Glucosamine-fructose-6-P amidotransferase is a substrate of TG2 transglutaminase activity
V. Modification of GFPT by TG2 enhances the hexosamine biosynthesis pathway
VI. TG2 activity controls the hexosamine biosynthetic pathway to provide the bacteria with UDP GlcNAc
I. C. trachomatis infection causes an increase in TG2 level and activity that benefits bacterial growth
II. TG2 is required to meet glucose demand during infection
III. TG2 exacerbates C. muridarum pathogenesis
IV. GFPT1, a substrate of TG2 activity
V. UDP-GlcNAc production is rapidly consumed in C. trachomatis infected cells
Concluding remarks
BIBLIOGRAPHY
