MicroRNA Let-7 in B lymphocyte activation
- Creators
- Jiang, Shuai
- Yan, Wei
- Wang, Shizhen Emily
Abstract
Over the past twenty years, mounting evidence showed that microRNA (miR) plays indispensable roles in various biological processes including aging process, immune cell responses and metabolic reprogramming through posttranscriptional gene targeting [1]. MiR-encoding genes are distributed in different chromosomes as individual genes or in clusters in human and murine genome [1]. Each miR cluster encodes at least two miRs that sometimes belong to the same family, making it critical to dissect the physiological and pathological roles of each clustered miR vs. the entire gene cluster in a given cellular context, such as B cells. Let-7 was one of the two ancient miRs initially found in C. elegans as a regulator of developmental timing [2]. The Let-7 family has twelve members which are distributed on seven different chromosomes in murine genome. Interestingly, all twelve members share the same "seed sequence", which is key to the complementation between miR and its target genes [3]. An intriguing question is why evolutionarily there are so many members in the let-7 family sharing the exactly same seed sequence. Do they play individual or redundant roles in various cellular context? Our recent work using transgenic mouse models of different let-7 family members revealed that some let-7 miRs express widely in differentiated immune cells including activated splenic B cells (4). We found that let-7a, let-7d, and let-7f were induced by LPS in splenic B cells, and that the let-7adf cluster inhibited B cell activation, whereas let-7e and let-7g were significantly decreased by LPS [4]. Based on these findings, we speculate that let-7e and let-7g might have unique functions compared to the let-7adf cluster in activated splenic B cells. Future experiments with overexpression or deletion of singular let-7e or let-7g by using engineered mouse models are essential to determine their physiological roles in B cells.
Additional Information
© 2019 Jiang et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Received: April 25, 2019 ; published: May 11, 2019.Attached Files
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Additional details
- PMCID
- PMC6535053
- Eprint ID
- 95594
- Resolver ID
- CaltechAUTHORS:20190520-094036263
- Created
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2019-05-20Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field