Effect of host fatty acid-binding protein and fatty acid uptake on growth of Chlamydia trachomatis L2

Wang, Guqi; Burczynski, Frank J.; Anderson, Judy E.; Zhong, Guangming

doi:10.1099/mic.0.2006/003491-0

Cited by 10 publications

(12 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Fatty acid synthesis is an energy-intensive process (10), and the energetic advantage of scavenging fatty acids from the host is obvious. Supplementing cells engineered to overexpress fatty acid binding protein with palmitate increased the titers of C. trachomatis (39), consistent with the energy-saving view of fatty acid scavenging. However, this process is constrained to not significantly perturb the production of predominately disaturated phospholipid molecular species C. trachomatis utilizes to construct its membrane systems.…”

Section: Discussionsupporting

confidence: 68%

Chlamydia trachomatis Scavenges Host Fatty Acids for Phospholipid Synthesis via an Acyl-Acyl Carrier Protein Synthetase

Yao

Dodson

Frank

et al. 2015

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: C. trachomatis relies on its own biosynthetic pathways to produce membrane phospholipids. Results: C. trachomatis expresses an acyl-acyl carrier protein synthetase to activate fatty acids. Conclusion: C. trachomatis utilizes fatty acids obtained from the host to construct phospholipids. Significance: C. trachomatis selectively scavenges host saturated fatty acids, the most energy-expensive component needed for phospholipid synthesis.

show abstract

Section: Discussionsupporting

confidence: 68%

Chlamydia trachomatis Scavenges Host Fatty Acids for Phospholipid Synthesis via an Acyl-Acyl Carrier Protein Synthetase

Yao

Dodson

Frank

et al. 2015

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Chlamydia places a large metabolic burden on its host cell, as revealed by increased rates of mitochondrial respiration (26) and long-chain fatty acid (LCFA) uptake (27). Because LDs are a rich source of esterified LCFA and LCFAs play a central role as high-energy substrates and precursors in PL biosynthesis, it is perhaps not surprising that C. trachomatis would have evolved mechanisms to take advantage of these organelles.…”

Section: Discussionmentioning

confidence: 99%

Cytoplasmic lipid droplets are translocated into the lumen of the Chlamydia trachomatis parasitophorous vacuole

Cocchiaro

Kumar

Fischer³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

275

328

View full text Add to dashboard Cite

The acquisition of host-derived lipids is essential for the pathogenesis of the obligate intracellular bacteria Chlamydia trachomatis. Current models of chlamydial lipid acquisition center on the fusion of Golgi-derived exocytic vesicles and endosomal multivesicular bodies with the bacteria-containing parasitophorous vacuole (''inclusion''). In this study, we describe a mechanism of lipid acquisition and organelle subversion by C. trachomatis. We show by live cell fluorescence microscopy and electron microscopy that lipid droplets (LDs), neutral lipid storage organelles, are translocated from the host cytoplasm into the inclusion lumen. LDs dock at the surface of the inclusion, penetrate the inclusion membrane and intimately associate with reticulate Bodies, the replicative form of Chlamydia. The inclusion membrane protein IncA, but not other inclusion membrane proteins, cofractionated with LDs and accumulated in the inclusion lumen. Therefore, we postulate that the translocation of LDs may occur at IncA-enriched subdomains of the inclusion membrane. Finally, the chlamydial protein Lda3 may participate in the cooption of these organelles by linking cytoplasmic LDs to inclusion membranes and promoting the removal of the LD protective coat protein, adipocyte differentiation related protein (ADRP). The wholesale transport of LDs into the lumen of a parasitophorous vacuole represents a unique mechanism of organelle sequestration and subversion by a bacterial pathogen.ADRP ͉ inclusion ͉ Lda3 ͉ organelle translocation

show abstract

“…Lipid transfer is facilitated by the close association of the C. trachomatis inclusion with host organelles such as the endoplasmic reticulum (23,(27)(28)(29)(30) and multivesicular bodies (31)(32)(33). C. trachomatis is also proposed to utilize host lipid droplets and fatty acid-binding proteins to assimilate lipids (24,34,35). A functioning inclusion membrane is critical to C. trachomatis proliferation, so it is not clear whether the lower C. trachomatis titers observed when lipid trafficking is inhibited arise from insufficient lipid for C. trachomatis and/or inclusion membrane formation.…”

mentioning

confidence: 99%

Chlamydia trachomatis Relies on Autonomous Phospholipid Synthesis for Membrane Biogenesis

Yao

Cherian

Frank

et al. 2015

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: C. trachomatis has a reduced genome and was thought to obtain phospholipids as well as other nutrients from the host. Results:The new phospholipid molecular species that appear in infected cells are produced by C. trachomatis. Conclusion: C. trachomatis needs only glucose, isoleucine, and serine to synthesize its own membrane phospholipids. Significance: C. trachomatis relies on autonomous phospholipid synthesis.

show abstract

Effect of host fatty acid-binding protein and fatty acid uptake on growth of Chlamydia trachomatis L2

Cited by 10 publications

References 31 publications

Chlamydia trachomatis Scavenges Host Fatty Acids for Phospholipid Synthesis via an Acyl-Acyl Carrier Protein Synthetase

Chlamydia trachomatis Scavenges Host Fatty Acids for Phospholipid Synthesis via an Acyl-Acyl Carrier Protein Synthetase

Cytoplasmic lipid droplets are translocated into the lumen of the Chlamydia trachomatis parasitophorous vacuole

Chlamydia trachomatis Relies on Autonomous Phospholipid Synthesis for Membrane Biogenesis

Contact Info

Product

Resources

About