دورية أكاديمية

Understanding the Function and Mechanism of Zebrafish Tmem39b in Regulating Cold Resistance

التفاصيل البيبلوغرافية
العنوان: Understanding the Function and Mechanism of Zebrafish Tmem39b in Regulating Cold Resistance
المؤلفون: Renyan Liu, Yong Long, Ran Liu, Guili Song, Qing Li, Huawei Yan, Zongbin Cui
المصدر: International Journal of Molecular Sciences, Vol 23, Iss 19, p 11442 (2022)
بيانات النشر: MDPI AG, 2022.
سنة النشر: 2022
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: cold resistance, zebrafish, tmem39b, tissue damage, immune response, damage repair, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: Autophagy and endoplasmic reticulum (ER) stress response are among the key pathways regulating cold resistance of fish through eliminating damaged cellular components and facilitating the restoration of cell homeostasis upon exposure to acute cold stress. The transmembrane protein 39A (TMEM39A) was reported to regulate both autophagy and ER stress response, but its vertebrate-specific paralog, the transmembrane protein 39B (TMEM39B), has not been characterized. In the current study, we generate tmem39b-knockout zebrafish lines and characterize their survival ability under acute cold stress. We observed that the dysfunction of Tmem39b remarkably decreased the cold resilience of both the larval and adult zebrafish. Gene transcription in the larvae exposed to cold stress and rewarming were characterized by RNA sequencing (RNA-seq) to explore the mechanisms underlying functions of Tmem39b in regulating cold resistance. The results indicate that the deficiency of Tmem39b attenuates the up-regulation of both cold- and rewarming-induced genes. The cold-induced transcription factor genes bif1.2, fosab, and egr1, and the rewarming-activated immune genes c3a.3, il11a, and sting1 are the representatives influenced by Tmem39b dysfunction. However, the loss of tmem39b has little effect on the transcription of the ER stress response- and autophagy-related genes. The measurements of the phosphorylated H2A histone family member X (at Ser 139, abbreviated as γH2AX) demonstrate that zebrafish Tmem39b protects the cells against DNA damage caused by exposure to the cold-warming stress and facilitates tissue damage repair during the recovery phase. The gene modules underlying the functions of Tmem39b in zebrafish are highly enriched in biological processes associated with immune response. The dysfunction of Tmem39b also attenuates the up-regulation of tissue C-reactive protein (CRP) content upon rewarming. Together, our data shed new light on the function and mechanism of Tmem39b in regulating the cold resistance of fish.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
1661-6596
Relation: https://www.mdpi.com/1422-0067/23/19/11442; https://doaj.org/toc/1661-6596; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms231911442
URL الوصول: https://doaj.org/article/ccb4e00db90346748949d8827d5beb20
رقم الأكسشن: edsdoj.b4e00db90346748949d8827d5beb20
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
16616596
DOI:10.3390/ijms231911442