Premium
TMED2 is Sufficient for Trophoblast Fusion
Author(s) -
JeromeMajewska Loydie,
Yuan Libin,
Hou wenyang,
Deba Taghreed
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb34
Subject(s) - syncytiotrophoblast , cell fusion , microbiology and biotechnology , syncytium , cytotrophoblast , gene knockdown , trophoblast , chemistry , biology , cell culture , placenta , fetus , genetics , pregnancy
TMED2 is essential for anterograde transport from the endoplasmic reticulum to the Golgi. We identified a protein null mutation in Tmed2 . At embryonic day (E) 9.5, Tmed2 homozygous ( Tmed2 99J/99J ) mutant embryos have abnormal placental labyrinth layer formation and fail to form the functional syncytiotrophoblast cells required for placental labyrinth layer formation, and die by E11.5. Tmed2 is expressed in mouse placenta and in human placentas, suggesting that TMED2 function is conserved in human and mouse placentas. We hypothesized that TMED2 was required for syncytiotrophoblast differentiation. We used qRT‐PCR to show that expression of TMED2 significantly increased when BeWo choriocarcinoma cells are induced to form syncytiotrophoblast. Furthermore, knockdown of TMED2 in this cell line does change the fusion index in the absence of Forskolin and but results in decreased metabolic activity when measured by MTT. To test for a direct role for TMED2 in syncytiotrophoblast formation, we generated JEG‐3 stable cell lines expressing TMED2myc. JEG‐3 cells do not normally fused but we will show that co‐culture of JEG‐3 stable cell lines expressing cytoplasmic GFP or mCherry allowed visualization of fusion. Quantification of syncytiotrophoblast fusion shows a significant increase in the fusion index of JEG‐3 cells, with no changes in metabolic activity by MTT. Our data suggest that TMED2 is sufficient for syncytiotrophoblast fusion.