What is it about?
For most of the pregnancy period, the smooth muscle cells of the uterus are not able to contract together. Labor begins when these cells become highly connected by special channels called gap junctions. These channels allow the cells to operate as a unit and undergo sustained and synchronous contractions that push out the baby. Our research question asked what causes uterine cells to create these gap junctions before labor commences. In this article, we link the presence of two proteins – MYB and ELF3 – to the control of gap junction production in uterine smooth muscle cells. Despite the strong expression of the Myb and Elf3 genes in the laboring uterus, we unexpectedly found that their proteins induce opposite effects on contraction-driving genes. We show that the presence of MYB results in increased activity of gap junction gene promoters. By contrast, ELF3 overrides the activation of these gene promoters, which may in turn stop labor contractions.
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Why is it important?
Understanding how genes that cause contractions are regulated at a molecular level can help us develop more effective means of preventing labor from initiating too soon. Premature birth, which occurs when a baby is born before the 37th week of pregnancy, can pose dangers for the infant because important developmental events, such as full maturation of the lungs, take place close to the end of term. Effective treatments are lacking and, as a result, premature birth remains a leading cause of illness and death for newborns around the world. Those babies who do survive often have to stay in the NICU for an extended period of time, which is hard on both the baby and the parents.
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This page is a summary of: MYB and ELF3 differentially modulate labor-inducing gene expression in myometrial cells, PLoS ONE, January 2023, PLOS,
DOI: 10.1371/journal.pone.0271081.
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