Hijacking of the nucleolar protein fibrillarin by TGB1 is required for cell‐to‐cell movement of Barley stripe mosaic virus

Barley stripe mosaic virus (BSMV) Triple Gene Block1 (TGB1) is a multifunctional movement protein with RNA‐binding, ATPase and helicase activities which mainly localizes to the plasmodesmata (PD) in infected cells. Here, we show that TGB1 localizes to the nucleus and the nucleolus, as well as the cytoplasm, and that TGB1 nuclear‐cytoplasmic trafficking is required for BSMV cell‐to‐cell movement. Prediction analyses and laser scanning confocal microscopy (LSCM) experiments verified that TGB1 possesses a nucleolar localization signal (NoLS) (amino acids 95–104) and a nuclear localization signal (NLS) (amino acids 227–238). NoLS mutations reduced BSMV cell‐to‐cell movement significantly, whereas NLS mutations almost completely abolished movement. Furthermore, neither the NoLS nor NLS mutant viruses could infect Nicotiana benthamiana systemically, although the NoLS mutant virus was able to establish systemic infections of barley. Protein interaction experiments demonstrated that TGB1 interacts directly with the glycine–arginine‐rich (GAR) domain of the nucleolar protein fibrillarin (Fib2). Moreover, in BSMV‐infected cells, Fib2 accumulation increased by about 60%–70% and co‐localized with TGB1 in the plasmodesmata. In addition, BSMV cell‐to‐cell movement in fib2 knockdown transgenic plants was reduced to less than one‐third of that of non‐transgenic plants. Fib2 also co‐localized with both TGB1 and BSMV RNA, which are the main components of the ribonucleoprotein (RNP) movement complex. Collectively, these results show that TGB1–Fib2 interactions play a direct role in cell‐to‐cell movement, and we propose that Fib2 is hijacked by BSMV TGB1 to form a BSMV RNP which functions in cell‐to‐cell movement.     

Lack of plasminogen leads to milk stasis and premature mammary gland involution during lactation

The extracellular serine protease, plasmin, is activated from its precursor, plasminogen (Plg), by the urokinase-type and tissue-type Plg activators (uPA and tPA respectively). One of the main plasmin substrates, fibrin, is formed from fibrinogen via thrombin activity. We have previously shown that mice deficient for Plg are strikingly less able to support a litter during lactation compared to wild type mice. Here we suggest a mechanism responsible for this lactation defect. Reduced epithelial content and increased apoptosis are observed in Plg-deficient mammary glands at lactation day 7. Immunofluorescence analysis reveals the presence of fibrin(ogen) in the stroma surrounding mammary alveoli and adipocytes and identifies fibrin(ogen) as a component of breast milk in both wild type and Plg-deficient mice. Furthermore, a large accumulation of fibrin(ogen) together with apoptotic epithelial cells is observed in the lactating mammary alveoli and ducts of some Plg-deficient mice. This suggests that fibrin plays a key role in the malfunction of mammary glands in the absence of Plg, possibly through blockade of mammary ducts inducing milk stasis, inhibiting milk expulsion and thereby inducing premature apoptosis and involution.     

ROC曲线评价Fib、CRP和NT-pro BNP在慢性房颤 并发早期心衰的诊断价值

目的：探讨CRP、Fib、NT-pro BNP在早期心衰患者中的诊断价值,并通过ROC曲线方法找到临床诊断界值。方法：对48 例 房颤并发早期心衰患者(A组),31 例为心房颤动并发重度心衰(B 组)和40 健康对照组(C 组)血清Fib、CRP 和NT-pro BNP水平。 利用ROC 曲线,评价CRP、Fib、NT-pro BNP 房颤并发早期心力衰竭诊断效能。结果：CRP、Fib 和NT-pro BNP 在B 组中水平最 高,C 组水平最低,三组间差异具有统计学意义(P<0.05)。NT-pro BNP 的对心房颤动并发早期心力衰竭患者诊断的灵敏度和特异 度明显高于Fib和CRP。NT-pro BNP 曲线下面积明显高于Fib 和CRP,差异有统计学意义(P>0.05)。结论：Fib、CRP 和NT-pro BNP在房颤并发可能或早期心衰患者血清中水平升高,联合诊断可以提高并发可能心衰的诊断敏感性,使得临床及早干预。     

冠心病患者的血脂、胆红素、UA及Fib水平变化及临床意义

目的:研究冠心病(CHD)患者的血脂、胆红素、血尿酸(UA)及纤维蛋白原(Fib)水平变化及临床意义。方法:选取2014年4月到2015年4月我院收治的CHD患者110例(研究组),另选取同期健康体检者110例(对照组),检测两组受检者血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、直接胆红素(DBIL)、间接胆红素(IBIL)、总胆固醇(TBIL)、UA以及Fib水平。结果:研究组TC、TG、LDL-C、UA以及Fib水平均显著高于对照组,两组比较差异具有统计学意义(P0.05);研究组HDL-C、DBIL、IBIL以及TBIL均显著低于对照组,两组比较差异具有统计学意义(P0.05)。结论:血脂水平异常,胆红素水平降低,UA以及Fib水平增高与CHD的发病有关。     

草生欧文氏菌(E.herbicola)CSH1065质粒的重组标记及Fib基因的遗传转移

利用DNA分子克隆技术及遗传重组方法,在E.herbicola CSH1065质粒上插入了Km_R及Mob基因,利用细菌间的接合转移,使E.herbicola CSH1065质粒转移到E.coli HB101中,从而获得了E.herbicola CSH1065的Fib(fungi inhibition)基因在E.coli HB101中的表达,进一步证明E.herbicola CSH1065 Fib基因功能只涉及其细胞内的大质粒,与其染色体基因组无关,其黄色色素基因与Fib功能无关。这些结果还为DNA分子杂交方法所证实。