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成年精子发生过程中同源结构域转录因子PKnox1/Prep1对生殖细胞的内在需求。

Germ cell-intrinsic requirement for the homeodomain transcription factor PKnox1/Prep1 in adult spermatogenesis.

作者信息

Kawai Yasuhiro, Oda Akihisa, Kanai Yoshiakira, Goitsuka Ryo

机构信息

Division of Development and Aging, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Chiba, Japan.

Department of Veterinary Anatomy, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.

出版信息

PLoS One. 2018 Jan 2;13(1):e0190702. doi: 10.1371/journal.pone.0190702. eCollection 2018.

DOI:10.1371/journal.pone.0190702
PMID:29293683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5749842/
Abstract

PKnox1 (also known as Prep1) belongs to the TALE family of homeodomain transcription factors that are critical for regulating growth and differentiation during embryonic and postnatal development in vertebrates. We demonstrate here that PKnox1 is required for adult spermatogenesis in a germ cell-intrinsic manner. Tamoxifen-mediated PKnox1 loss in the adult testes, as well as its germ cell-specific ablation, causes testis hypotrophy with germ cell apoptosis and, as a consequence, compromised spermatogenesis. In PKnox1-deficient testes, spermatogenesis was arrested at the c-Kit+ spermatogonia stage, with a complete loss of the meiotic spermatocytes, and was accompanied by compromised differentiation of the c-Kit+ spermatogonia. Taken together, these results indicate that PKnox1 is a critical regulator of maintenance and subsequent differentiation of the c-Kit+ stage of spermatogonia in the adult testes.

摘要

PKnox1(也称为Prep1)属于同源结构域转录因子的TALE家族,该家族对于脊椎动物胚胎期和出生后发育过程中的生长和分化调节至关重要。我们在此证明,PKnox1以生殖细胞内在方式参与成年期精子发生。他莫昔芬介导的成年睾丸中PKnox1缺失及其生殖细胞特异性消融,会导致睾丸萎缩并伴有生殖细胞凋亡,进而损害精子发生。在PKnox1缺陷型睾丸中,精子发生停滞在c-Kit +精原细胞阶段,减数分裂的精母细胞完全缺失,并伴有c-Kit +精原细胞分化受损。综上所述,这些结果表明PKnox1是成年睾丸中精原细胞c-Kit +阶段维持和后续分化的关键调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/f3a1ed8b4f59/pone.0190702.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/135b8227d5c3/pone.0190702.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/8f4940184c44/pone.0190702.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/5d31961e062b/pone.0190702.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/8a1dd7de1c0f/pone.0190702.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/340791dc4324/pone.0190702.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/f3a1ed8b4f59/pone.0190702.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/135b8227d5c3/pone.0190702.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/8f4940184c44/pone.0190702.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/5d31961e062b/pone.0190702.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/8a1dd7de1c0f/pone.0190702.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/340791dc4324/pone.0190702.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb65/5749842/f3a1ed8b4f59/pone.0190702.g006.jpg

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