Abstract
The early growth response (Egr) family of zinc finger transcription factors consists of 4 members. During an investigation of Egr factor localization in mouse ovaries, we noted that Egr3 exhibits a subcellular localization that overlaps with the meiotic spindle in oocytes. Using Egr3-specific antibodies, we establish that Egr3 co-localizes with the spindle and cytosolic microtubule organizing centers (MTOCs) in oocytes during meiotic maturation. Notably, the Egr3 protein appears to accumulate around γ-tubulin in MTOCs. Nocodazole treatment, which induces microtubule depolymerization, resulted in the disruption of spindle formation and Egr3 localization, suggesting that Egr3 localization is dependent on the correct configuration of the spindle. Shortly after warming of vitrified oocytes, growing arrays of microtubules were observed near large clusters of Egr3. An in vitro microtubule interaction assay showed that Egr3 does not directly interact with polymerized microtubules. Egr3 localization on the spindle was sustained in early preimplantation mouse embryos, but this pattern did not persist until the blastocyst stage. Collectively, our result shows for the first time that the Egr3 a transcription factor may play a novel non-transcriptional function during microtubule organization in mouse oocytes.
Highlights
The early growth response (Egr) family of zinc finger-containing transcription factors includes 4 members (Egr1–4) that participate in multiple physiological processes [1,2,3,4,5,6]
We performed Egr3 immunofluorescence staining in parallel with Egr1, 2, and 4, and found that Egr3 was the only member of the Egr family that exhibited this subcellular localization in the mouse ovary
The roles of Egr3 in muscle spindle morphogenesis and neurological functions have been established in a series of studies employing Egr3 deficient mice [3,9,27,28]
Summary
The early growth response (Egr) family of zinc finger-containing transcription factors includes 4 members (Egr1–4) that participate in multiple physiological processes [1,2,3,4,5,6]. Egr plays a wellestablished role in regulating the transcription of the luteinizing hormone b subunit gene [7] and hormone responsiveness in the ovary [8]. Egr deficient male mice are reportedly infertile, implicating Egr in male reproduction [11]. Consistent with this role, Egr is associated with the maintenance of the spermatogonia stem cell (SSC) pool in the rat testis [12]. An Egr family of protein in C. elegans, encoded by the early growth response homolog (egrh-1), plays a role in oocyte maturation and ovulation in the absence of sperm [13]
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