Researchers have found that a gene called Elf5, plays a critical role in developmental crossroad. Thus finding is likely to help the researchers to understand the process of fertilisation. It will ensure that cells either become committed to forming the placenta or the embryo.
The fertilised embryo possesses the greatest plasticity; it is totipotent and can differentiate into all cell types of the foetus as well as the placenta. One of the first definitive divergences in cell differentiation pathways is the point where cells that will form the placenta are set aside from those that will form the foetus. Once this decision has been made, it was thought that there is no turning back or crossover between future placental and embryonic cells. How this strict lineage separation is achieved, however, has remained elusive.
Since all cells in an individual contain the same genetic material, but behave differently depending on which organs eventually comprise, an elaborate mechanism has evolved to fine tune our genes and their expression in different places at different times, leading to the amazing complexity we see in humans despite the relatively small number of unique genes.
This work has provided new insights into the apparent irreversibility of cell fate and how cell fate is normally locked in to achieve stable differentiation. This is of particular importance for strategies in regenerative medicine that aim to generate a specific cell type from multi- or pluripotent stem cells and to prevent its de-differentiation, a process that bears the risk of tumour formation. Ultimately, these results may pave the way for differentiated cells to be specifically instructed to generate other essential cell types for therapeutic use. This knowledge will open up new possibilities into research of pregnancy complications that have a specific placental origin.
Dr Myriam Hemberger said,
“The DNA sequence of the gene Elf5 is modified by a methylation mark in future populations of embryonic cells ensuring that the gene is kept in a stable ‘off’ state. In contrast the sequence is not modified in placental cells; the gene is ‘on’ and reinforces placental cell fate. We demonstrated that by removing the methylation mark in embryonic cells, we could convert these normally committed embryonic cells into cells with placental characteristics.”
Source: innovations report