Abstract
Tristetraprolin (TTP), a member of TIS11 family containing CCCH tandem zinc finger, is one of the best characterized RNA-binding proteins. However, to date, the role of TTP in mammalian oocytes remains completely unknown. In the present study, we report the altered maturational progression and cytokinesis, upon specific knockdown of TTP in mouse oocytes. Furthermore, by confocal scanning, we observe the failure to form cortical actin cap during meiosis of TTP-depleted oocytes. Loss of TTP in oocytes also results in disruption of meiotic spindle morphology and chromosome alignment. In support of these findings, incidence of aneuploidy is accordingly increased when TTP is abated in oocytes. Our results suggest that TTP as a novel cytoskeletal regulator is required for spindle morphology/chromosome alignment and actin polymerization in oocytes.
Highlights
Tristetraprolin (TTP, ZFP36) is the founding member of tandem CCCH zinc fingers containing proteins that negatively regulates RNA stability, promotes RNA degradation
Our results suggest that TTP as a novel cytoskeletal regulator is required for spindle morphology/chromosome alignment and actin polymerization in oocytes
By immunofluorescent labeling coupled with confocal microscopy, we examined TTP distribution during mouse oocyte maturation
Summary
Tristetraprolin (TTP, ZFP36) is the founding member of tandem CCCH zinc fingers containing proteins that negatively regulates RNA stability, promotes RNA degradation. AREs are the important elements regulating posttranscription, and have been detected in around 10% of the human transcriptomes [2]. Since its discovery as a regulator of TNFα mRNA stability nearly two decades ago, TTP has become one of the best understood posttranscriptional regulators associated with tumors and inflammation [3, 4]. It has been showed that TTP regulates the expression of MyoD, CCL3 and IL-23 in an mRNAdecay dependent way [5,6,7,8]. Increased systemic levels of TTP, secondary to increased stability of its mRNA throughout the body, can protect mice against immunemediated inflammatory pathologies [9]. TTP can affect the balance of anabolic and catabolic gene expression in human chondrocytes [11]. It is worth noting that TTP is expressed in growing mouse oocytes [12], but its role in germ cells remains completely unknown
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