| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J. Biol. Chem., Vol. 277, Issue 49, 47701-47708, December 6, 2002
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
§¶
,¶,,§,§¶¶
From the Phosphatidylserine synthase
1 (Pss1) and phosphatidylserine synthase 2 (Pss2) produce
phosphatidylserine by exchanging serine for the head groups of other
phospholipids. Pss1 and Pss2 are structurally similar (~32% amino
acid identity) but differ in their substrate specificities, with Pss1
using phosphatidylcholine for the serine exchange reaction and Pss2
using phosphatidylethanolamine. Whether Pss1 and Pss2 are both required
for mammalian growth and development is not known, and no data exist on
the relative contributions of the two enzymes to serine exchange
activities in different tissues. To address those issues and also to
define the cell type-specific expression of Pss2, we
generated Pss2-deficient mice in which a Gladstone Institute of Cardiovascular
Disease, § Cardiovascular Research Institute, and
¶¶ Department of Medicine, University of California, San
Francisco, and the Medical Service, San Francisco General Hospital, San
Francisco, California 94110, the ** Canadian Institute for
Health Research Group on Molecular and Cell Biology of Lipids and
Department of Medicine, University of Alberta, Edmonton, Alberta T6G
2S2, Canada, the National Hormone and
Peptide Program, Harbor-UCLA Medical Center, Torrance, California
90509, and the §§ Department of Molecular and
Cell Biology, University of California,
Berkeley, California 94720
-galactosidase
marker is expressed from Pss2 regulatory sequences. Histologic studies of Pss2-deficient mice revealed very
high levels of -galactosidase expression in Sertoli cells of the
testis and high levels of expression in brown fat, neurons, and
myometrium. The ability of testis extracts from
Pss2-deficient mice to catalyze serine exchange was reduced
by more than 95%; reductions of ~90% were noted in the brain and
liver. However, we found no perturbations in the phospholipid content
of any of these tissues. As judged by Northern blots, the expression of
Pss1 was not up-regulated in Pss2-deficient
cells and tissues. Testis weight was reduced in
Pss2-deficient mice, and some of the male mice were
infertile. We conclude that Pss2 is responsible for the majority of
serine exchange activity in in vitro assays, but a
deficiency in this enzyme does not cause perturbations in phospholipid
content or severe developmental abnormalities.
To whom correspondence should be addressed: Gladstone
Institute of Cardiovascular Disease, P.O. Box 419100, San Francisco, CA
94141-9100. Tel.: 415-826-7500; Fax: 415-285-5632; E-mail: mbergo@gladstone.ucsf.edu.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  J. E. Vance Thematic Review Series: Glycerolipids. Phosphatidylserine and phosphatidylethanolamine in mammalian cells: two metabolically related aminophospholipids J. Lipid Res., July 1, 2008; 49(7): 1377 - 1387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Arikketh, R. Nelson, and J. E. Vance Defining the Importance of Phosphatidylserine Synthase-1 (PSS1): Unexpected Viability of PSS1-Deficient Mice J. Biol. Chem., May 9, 2008; 283(19): 12888 - 12897. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Lee, C. Shah, and E. Y. Xu Gene trap mutagenesis: a functional genomics approach towards reproductive research Mol. Hum. Reprod., November 1, 2007; 13(11): 771 - 779. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. D. Fullerton, F. Hakimuddin, and M. Bakovic Developmental and Metabolic Effects of Disruption of the Mouse CTP:Phosphoethanolamine Cytidylyltransferase Gene (Pcyt2) Mol. Cell. Biol., May 1, 2007; 27(9): 3327 - 3336. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Reue and L. Vergnes Thematic review series: Systems Biology Approaches to Metabolic and Cardiovascular Disorders. Approaches to lipid metabolism gene identification and characterization in the postgenomic era J. Lipid Res., September 1, 2006; 47(9): 1891 - 1907. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Iguchi, J. W. Tobias, and N. B. Hecht Expression profiling reveals meiotic male germ cell mRNAs that are translationally up- and down-regulated PNAS, May 16, 2006; 103(20): 7712 - 7717. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. B. Sher, C. Aoyama, K. A. Huebsch, S. Ji, J. Kerner, Y. Yang, W. N. Frankel, C. L. Hoppel, P. A. Wood, D. E. Vance, et al. A Rostrocaudal Muscular Dystrophy Caused by a Defect in Choline Kinase Beta, the First Enzyme in Phosphatidylcholine Biosynthesis J. Biol. Chem., February 24, 2006; 281(8): 4938 - 4948. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Steenbergen, T. S. Nanowski, A. Beigneux, A. Kulinski, S. G. Young, and J. E. Vance Disruption of the Phosphatidylserine Decarboxylase Gene in Mice Causes Embryonic Lethality and Mitochondrial Defects J. Biol. Chem., December 2, 2005; 280(48): 40032 - 40040. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Akbar, F. Calderon, Z. Wen, and H.-Y. Kim Docosahexaenoic acid: A positive modulator of Akt signaling in neuronal survival PNAS, August 2, 2005; 102(31): 10858 - 10863. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. E. Vance and D. E. Vance Metabolic Insights into Phospholipid Function Using Gene-targeted Mice J. Biol. Chem., March 25, 2005; 280(12): 10877 - 10880. [Full Text] [PDF]
|
|
|
|
|
|
R. L. Jacobs, C. Devlin, I. Tabas, and D. E. Vance Targeted Deletion of Hepatic CTP:phosphocholine Cytidylyltransferase {alpha} in Mice Decreases Plasma High Density and Very Low Density Lipoproteins J. Biol. Chem., November 5, 2004; 279(45): 47402 - 47410. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. P. Beigneux, C. Kosinski, B. Gavino, J. D. Horton, W. C. Skarnes, and S. G. Young ATP-Citrate Lyase Deficiency in the Mouse J. Biol. Chem., March 5, 2004; 279(10): 9557 - 9564. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. McMullen, T. Shioi, W.-Y. Huang, L. Zhang, O. Tarnavski, E. Bisping, M. Schinke, S. Kong, M. C. Sherwood, J. Brown, et al. The Insulin-like Growth Factor 1 Receptor Induces Physiological Heart Growth via the Phosphoinositide 3-Kinase(p110{alpha}) Pathway J. Biol. Chem., February 6, 2004; 279(6): 4782 - 4793. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
