User:Kroth2021/N6-Methyladenosine

Article body
Original: Several more recent studies have revealed that m6A regulators govern the efficiency of infection and replication of RNA viruses such as human immunodeficiency virus (HIV), hepatitis C virus (HCV), and Zika virus (ZIKV).

Edited: Several more recent studies have revealed that m6A regulators govern the efficiency of infection, replication, translation and transport of RNA viruses such as human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Zika virus (ZIKV).

New Paragraph: Aside from affecting viruses themselves, m6A modifications can also disrupt the innate immune response. For example, in HBV, m6A modifications were shown to disrupt the recognition of viruses by RIG-1, a pattern recognition receptor in the immune system. Modifications can also disrupt downstream signaling pathways via mechanisms including ubiquitination and changes in the levels of protein expression.

New Section/Paragraph: Put after "In Bacteria" section

In Development
m6A modifications, along with other epigenetic changes, have been shown to play important roles during eukaryotic development. Hematopoietic Stem Cells (HSCs), Neuronal Stem Cells (NSCs) and Primordial Germ Cells (PCGs) have all been shown to undergo m6A modifications during growth and differentiation. Depending on the stage of development, modifications to HSCs can either promote or inhibit stem cell differentiation by affecting the epithelial-to-hemopoietic transition via METTL3 inhibition or depletion. m6A modifications to NSCs can causes changes in brain size, neuron formation, long-term memory, and learning ability. These changes are often caused by inhibition of either METTL or YTHDF readers and writers. In the reproductive system, m6A modifications have been shown to disrupt the maternal-to-zygotic mRNA transition and negatively affect both gamete formation and fertility. Similar to NSCs, inhibition of the METTL and YTHDF families of proteins is often a catalyst for these changes.