近日,，哈爾濱工業(yè)大學(xué)生命科學(xué)學(xué)院合約研究員劉北東、博士生宋佳和楊曉雪關(guān)于SIR2基因的研究取得了重大成果,，研究論文《細(xì)胞蛋白聚合體的隔離與細(xì)胞肌動(dòng)蛋白和極化機(jī)制相關(guān)》發(fā)表在最新一期的《細(xì)胞》（Cell）雜志。國(guó)際同行認(rèn)為，該成果對(duì)衰老和神經(jīng)細(xì)胞退化性疾病的研究有重要意義,。
劉北東等人根據(jù)觀察到的蛋白聚合體在細(xì)胞中形成的穩(wěn)定纖維結(jié)構(gòu)與肌動(dòng)蛋白骨架結(jié)構(gòu)位置重合、敲除細(xì)胞極化機(jī)制導(dǎo)致細(xì)胞蛋白聚合體的隔離缺失等現(xiàn)象,，進(jìn)一步證實(shí)了蛋白聚合體的隔離是肌動(dòng)蛋白和極化機(jī)制所參與的主動(dòng)過(guò)程,。此發(fā)現(xiàn)糾正了以往認(rèn)為該隔離機(jī)制是一個(gè)完全被動(dòng)過(guò)程的看法。
劉北東一直致力于微生物技術(shù)研究,。2010年,，其論文《細(xì)胞極化體是受損蛋白聚合體在細(xì)胞內(nèi)隔離和逆向傳輸?shù)闹匾蜃印吩凇都?xì)胞》雜志發(fā)表,，被認(rèn)為在酵母菌細(xì)胞內(nèi)發(fā)現(xiàn)了一個(gè)嶄新的生物過(guò)程，該過(guò)程對(duì)生物體的衰老和后代的衰老時(shí)鐘的重新設(shè)定起重要作用,；國(guó)際權(quán)威學(xué)者還在同期雜志撰文予以高度評(píng)價(jià),。（生物谷Bioon.com）
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doi:10.1016/j.cell.2011.11.018
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Segregation of Protein Aggregates Involves Actin and the Polarity Machinery
Beidong Liu, Lisa Larsson, Vanessa Franssens, Xinxin Hao, Sandra Malmgren Hill, Veronica Andersson, Daniel Höglund, Jia Song, Xiaoxue Yang, David Öling et al.
Cells of yeast to mammals have evolved the means of spatial quality control (SQC), which includes the transport of protein aggregates on microtubules into a structure called the aggresome (Kopito, 2000,Wang et al., 2009) and a factor-dependent compartmentalization of aggregates into juxtanuclear sites (JUNQ) and perivacuolar inclusions (IPOD) (Kaganovich et al., 2008). SQC also encompasses an actin cytoskeleton-, polarisome-, and Hsp104-dependent segregation of damaged proteins during yeast cytokinesis (Aguilaniu et al., 2003,Erjavec et al., 2007,Tessarz et al., 2009). In addition, some aggregates in yeast daughter cells were observed to move (retrograde) into the mother cell after a transient heat stress (Liu et al., 2010). In this issue of Cell, Zhou et al., 2011 now extend this analysis and, with the aid of theoretical simulations, suggest that motility of protein aggregates is characterized by random and slow diffusion, completely devoid of directional bias. Further, it is argued that aggregate asymmetry is established in a purely passive and random manner and that no active, factor-dependent (e.g., polarisome) mechanism is involved in conferring SQC. This model contrasts that of Tessarz et al., 2009 and Liu et al., 2010, which both interpret the failure of mutants with defects in polarisome and Hsp104 functions to establish damage asymmetry indicative of damage retention being a factor-dependent process.
When considering the different views on the establishment of damage asymmetry, it should be pointed out that measurements aimed at determining the frequency of aggregate movement between mother and daughter should only include budding events in which such transfer is physically possible. This is the case during the S to early G2 phase, when the polarisome is localized at the bud tip and actin cables extend from the bud into the mother compartment. When these phases are considered, our data show that there is a bias toward retrograde movement of aggregates from daughter to mother. In 393 budding events analyzed (between 56 and 84 such events were analyzed in the Zhou et al. study), we found that 15.5% showed cross-compartment movements (Figure 1A), and among these, retrograde movement from bud to mother (66.5%) is significantly more frequent than anterograde movement (25.4%; p = 0.03) and movement in both directions (8.1%; p = 0.007) (Figure 1B). Figure S1 in the Supplemental Information available online shows two budding events with simultaneously retrograde movement of aggregates (Movie S1. An Uncropped Full-Field Movie Showing Several Budding Events with Retrograde Movement is an uncropped full-field movie showing several retrograde movements).
