单亲和多倍体胚泡的机制起源和植入前发育

Yan Zhao, Andrea Fernández-Montoro, Greet Peeters, Tatjana Jatsenko, Tine De Coster, Daniel Angel-Velez, Thomas Lefevre, Thierry Voet, Olga Tšuiko, Ants Kurg, Katrien Smits, Ann Van Soom, Joris Robert Vermeesch
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引用次数: 0

摘要

全基因组(WG)异常,如单亲二倍体和三倍体,会导致胎儿死亡。在活产中,它们偶尔会与双亲二倍体细胞共存。了解 WG 异常胚泡的起源和早期发育,对于解释雄激素、雌激素、三倍体、嵌合体和混合倍性的形成至关重要。通过对来自第一裂殖的 118 个胚泡进行单倍型分析,我们确定了导致 WG 异常胚泡或在多极性和双极性裂殖合子中与正常胚泡共存的各种异源分裂机制。在将全能胚泡培养到三个植入前阶段并对 600 多个细胞进行转录组分析后,我们发现应激反应导致 WG 异常细胞发育受损,导致细胞停滞或胚泡形成。然而,第一次裂解衍生的 WG 异常胚泡能在早期发育中存活下来并发育成胚泡。它们在植入前胚胎中的潜在优势是被忽视的异常发育原因。基于单倍型的筛查可进一步提高妊娠率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanistic origin and preimplantation development of uniparental and polyploid blastomeres
Whole-genome (WG) abnormalities, such as uniparental diploidy and triploidy, cause fetal death. Occasionally, they coexist with biparental diploid cells in live births. Understanding the origin and early development of WG abnormal blastomeres is crucial for explaining the formation of androgenotes, gynogenotes, triploidy, chimerism, and mixoploidy. By haplotyping 118 blastomeres from first cleavages, we identified various mechanisms of heterogoneic divisions that lead to WG abnormal blastomeres or their coexistence with normal blastomeres in both multipolar and bipolar cleaving zygotes. After culturing the totipotent blastomeres to three preimplantation stages and performing transcriptome profiling on over 600 cells, we discovered that stress responses contribute to developmental impairment in WG abnormal cells, resulting in either cell arrest or blastocyst formation. However, first-cleavage-derived WG abnormal blastomeres can survive early development and progress to blastocysts. Their potential dominance in preimplantation embryos represents an overlooked cause of abnormal development. Haplotype based screening could further increase pregnancy rates.
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