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Treacher Collins综合征中新型TCOF1突变的鉴定及其功能特征分析

Identification of novel TCOF1 mutations in Treacher Collins syndrome and their functional characterization.

作者信息

Chen Ying, Yang Run, Chen Xin, Zhang Tianyu, Li Chenlong, Ma Jing

机构信息

Department of Facial Plastic and Reconstructive Surgery, ENT Institute, Eye and ENT Hospital of Fudan University, Shanghai, 200031, People's Republic of China.

NHC Key Laboratory of Hearing Medicine, Fudan University, Shanghai, 200031, People's Republic of China.

出版信息

Orphanet J Rare Dis. 2025 Apr 16;20(1):184. doi: 10.1186/s13023-025-03667-7.

Abstract

BACKGROUND

Treacher Collins syndrome (TCS) is a congenital disorder primarily caused by the mutation in the Treacle Ribosome Biogenesis Factor 1 (TCOF1) gene. However, the significance of many TCOF1 mutations remains uncertain.

RESULTS

We report two novel mutations identified in two TCS families and assess their pathogenicity alongside two previously reported mutations. Both novel mutations, c.2115dupG (p.T706DfsTer52) and c.2142+23_2142+52 del (p.A715VfsTer31), result in truncated proteins lacking nuclear location signals (NLSs), which impedes their entry into the nucleus and reduces mRNA expression level. Notably, the mutation c.2142+23_2142+52 del, leading to the retention of a 62 bp intron and disrupting RNA splicing, represents the first documented case of intron retention in TCS patients. Additionally, the previously reported mutation c.136 C> G (p.L46V) hinders protein nuclear location, while mutation c.1719del (p.N574TfsTer22) significantly decreases mRNA levels.

CONCLUSIONS

Our research expands the spectrum of TCOF1 mutations and provides evidence clarifying their pathogenic nature. These findings are crucial for genetic counseling and prenatal diagnosis for TCS patients.

摘要

背景

特雷彻·柯林斯综合征(TCS)是一种先天性疾病,主要由Treacle核糖体生物合成因子1(TCOF1)基因突变引起。然而,许多TCOF1突变的意义仍不明确。

结果

我们报告了在两个TCS家族中鉴定出的两个新突变,并与之前报道的两个突变一起评估了它们的致病性。这两个新突变,即c.2115dupG(p.T706DfsTer52)和c.2142+23_2142+52 del(p.A715VfsTer31),均导致缺乏核定位信号(NLSs)的截短蛋白,这阻碍了它们进入细胞核并降低了mRNA表达水平。值得注意的是,突变c.2142+23_2142+52 del导致保留了一个62 bp的内含子并破坏了RNA剪接,这是TCS患者中首次有记录的内含子保留病例。此外,之前报道的突变c.136 C>G(p.L46V)阻碍了蛋白的核定位,而突变c.1719del(p.N574TfsTer22)显著降低了mRNA水平。

结论

我们的研究扩展了TCOF1突变谱,并提供了阐明其致病性质的证据。这些发现对于TCS患者的遗传咨询和产前诊断至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89cf/12001626/0398279fa920/13023_2025_3667_Fig1_HTML.jpg

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