In vivo function and evolution of the eutherian-specific pluripotency marker UTF1
Masazumi Nishimoto1, Miyuki Katano, Toshiyuki Yamagishi
1Radioisotope Experimental Laboratory, Research Center for Genomic Medicine, Saitama Medical University, Yamane Hidaka, Saitama, Japan. masamasa@saitama-med.ac.jp
Plos One
|July 23, 2013
Summary
Loss of the UTF1 gene in mice causes smaller newborns due to placental insufficiency. This gene, found only in placental mammals, may have evolved to support pregnancy.
Area of Science:
- Developmental Biology
- Genetics
- Evolutionary Biology
Background:
- Embryogenesis in placental mammals relies on complex interactions between the embryo and placenta.
- UTF1 is a gene crucial for development, expressed in both embryonic and placental cells.
Purpose of the Study:
- To investigate the developmental consequences of UTF1 gene loss in mice.
- To explore the evolutionary origin and potential function of UTF1 in placental mammals.
Main Methods:
- Analysis of homozygous UTF1 mutant mice.
- Comparison of wild-type and heterozygous mutant mice.
- Genome structure and sequence analysis of UTF1 and homologous genes.
Main Results:
- Homozygous UTF1 mutant newborn mice exhibited significantly reduced size compared to controls.
- Placental insufficiency, resulting from UTF1 loss in extra-embryonic ectoderm, contributed to the observed growth phenotype.
- Loss of UTF1 in embryonic stem cells had minimal impact on pluripotency.
- The UTF1 gene is unique to placental mammals, with homologous genes suggesting an evolutionary pathway.
Conclusions:
- UTF1 plays a critical role in mammalian placental development and fetal growth.
- The evolution of UTF1 is linked to the adaptation of pregnancy in placental mammals.
- Further research into UTF1's precise mechanisms in placental development is warranted.
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