國家英才計劃(生物）于12月7日結(jié)束，北京海淀稻香湖學(xué)校學(xué)生張閎熙再創(chuàng)佳績，獲得了國家優(yōu)秀學(xué)員，生物組順位第一，同輩評議第一，并獲取了參加中國對外交流遴選營資格的輝煌成績。

The National Talent Program(Biology)ended on December 7th,and Zhang Hongxi,a student from Beijing Daoxianghu School,achieved remarkable results.He was awarded the title of National Excellent Student,ranked first in the Biology Group,and ranked first in peer evaluation.He also achieved brilliant results in qualifying for China's Foreign Exchange Selection Camp.

什么是國家英才計劃？

國家英才計劃直屬于中國科技協(xié)會，是我國高中生超前培養(yǎng)的重要平臺。“英才計劃”旨在選拔一批學(xué)有余力的中學(xué)生走進(jìn)大學(xué)，在自然科學(xué)基礎(chǔ)學(xué)科領(lǐng)域的著名學(xué)者指導(dǎo)下參加科學(xué)研究、學(xué)術(shù)研討和科研實踐，進(jìn)而發(fā)現(xiàn)一批具有學(xué)科特長、創(chuàng)新潛質(zhì)的優(yōu)秀中學(xué)生，提前促進(jìn)學(xué)生與大學(xué)教育相銜接，建立高校與中學(xué)聯(lián)合發(fā)現(xiàn)和培養(yǎng)頂尖科技創(chuàng)新人才的有效模式，為青少年科技創(chuàng)新人才不斷涌現(xiàn)和成長營造良好的社會氛圍。

The National Talent Program is directly affiliated with the China Association of Science and Technology and is an important platform for advanced training of high school students in China.The"Talent Plan"aims to select a group of high school students who have spare energy to enter universities,participate in scientific research,academic seminars,and research practices under the guidance of renowned scholars in the field of natural science basic disciplines,and discover a group of outstanding high school students with disciplinary strengths and innovative potential.It promotes the connection between students and university education in advance,and establishes an effective model for universities and high schools to jointly discover and cultivate top scientific and technological innovation talents,To create a favorable social atmosphere for the continuous emergence and growth of young technological innovation talents.

英才計劃的審核有多嚴(yán)格？

初選:在全國優(yōu)秀高中中選拔7000位學(xué)生參加英才計劃的資格考試，取1500名學(xué)生進(jìn)入英才計劃（筆試兩輪+一輪面試）

中期評估：學(xué)生進(jìn)入課題組后由中國科協(xié)審核每月的成長記錄和演技筆記，不合格者退出英才計劃。

終期評估：學(xué)生提交課題報告、培養(yǎng)報告(包括讀書報告、文獻(xiàn)綜述、實驗記錄、論文等)、《成長日志》、導(dǎo)師評價等材料。中國科協(xié)篩選后選取150人參加最終評估（前10%），最后留下30人（前2%）推送至中國對外交流遴選營。生物組評委組組長擔(dān)任者為中國科學(xué)院院士，普林斯頓大學(xué)生物系終身教授，西湖大學(xué)校長施一公先生，評委組共12位生物領(lǐng)域著名學(xué)者構(gòu)成，經(jīng)過四輪密閉交叉答辯得出最后結(jié)果。

Preliminary selection:7000 students will be selected from the national excellent high schools to participate in the qualification exam of the Talent Program,and 1500 students will be selected to enter the Talent Program(two rounds of written exams and one round of interviews)

Mid term evaluation:After entering the research group,students will have their monthly growth records and acting notes reviewed by the China Association for Science and Technology.Those who fail will be expelled from the Talent Program.

Final evaluation:Students submit project reports,training reports(including reading reports,literature reviews,experimental records,papers,etc.),growth logs,mentor evaluations,and other materials.After screening by the China Association for Science and Technology,150 people were selected to participate in the final evaluation(the top 10%),and 30 people(the top 2%)were left to be pushed to the China Foreign Exchange Selection Camp.The leader of the jury group of the biology group is Shi Yigong,an academician of the CAS Member,a tenured professor of the Department of Biology of Princeton University,and the president of West Lake University.The jury group consists of 12 famous scholars in the field of biology.After four rounds of closed cross defense,the final result was obtained.

獲獎?wù)n題：

鐵轉(zhuǎn)運蛋白基因X調(diào)控髓鞘形成和少突膠質(zhì)細(xì)胞發(fā)育的機(jī)理

The mechanism of iron transporter gene X regulating myelin formation and oligodendrocyte development

摘要：

溶質(zhì)載體家族(SLCs)作為最大的轉(zhuǎn)運蛋白家族，在細(xì)胞膜上控制著包括糖類、無機(jī)鹽、氨基酸、神經(jīng)遞質(zhì)、維生素、ATP等在內(nèi)的多種細(xì)胞生長所必須的物質(zhì)的轉(zhuǎn)運。SLCs參與這些細(xì)胞的生長發(fā)育，其功能異常常常與人類健康和疾病息息相關(guān)。基因X是識別鐵載體從而實現(xiàn)鐵的跨膜運輸。雖然已經(jīng)有研究表明其在中樞神經(jīng)系統(tǒng)尤其是少突膠質(zhì)細(xì)胞上高表達(dá)，但是基因X在少突膠質(zhì)細(xì)胞內(nèi)的生理功能和參與髓鞘形成過程的潛在機(jī)制仍然是未解之謎。本文從髓鞘發(fā)育和再生的角度詳細(xì)闡述了基因X在少突膠質(zhì)細(xì)胞中的特異性敲除嚴(yán)重影響了中樞神經(jīng)系統(tǒng)中的髓鞘形成，這種髓鞘障礙還同時伴隨著少突膠質(zhì)細(xì)胞的分化受阻。考慮到基因X是一類參與鐵運輸?shù)霓D(zhuǎn)運蛋白，而少突膠質(zhì)細(xì)胞的鐵積累是其分化所必須的，因此我們建立了高鐵小鼠模型來探究基因X在少突膠質(zhì)細(xì)胞中的作用是否與其轉(zhuǎn)鐵功能相關(guān)。食物中補(bǔ)充的大量鐵能夠促進(jìn)髓鞘形成和少突膠質(zhì)細(xì)胞分化進(jìn)程，然而當(dāng)基因X缺失這一促進(jìn)作用明顯減弱，這一結(jié)果提示我們基因X可能是通過調(diào)控少突膠質(zhì)細(xì)胞的鐵轉(zhuǎn)運來影響其分化。少突膠質(zhì)細(xì)胞發(fā)育障礙導(dǎo)致了多種脫髓鞘神經(jīng)系統(tǒng)疾病如多發(fā)性硬化癥(MS)等的內(nèi)源性髓鞘再生失敗，探究基因X介導(dǎo)的鐵轉(zhuǎn)運機(jī)制可能成為治療此類疾病的潛在思路。

The solute carrier family(SLCs),as the largest transporter protein family,control the cell membrane including sugars.Various substances necessary for cell growth,including inorganic salts,amino acids,neurotransmitters,vitamins,ATP,etc.The transfer of quality.SLCs are involved in the growth and development of these cells,and their abnormal functions are often closely related to human health and diseases.Gene X recognizes iron carriers to achieve transmembrane transport of iron.Although there have been studies indicating its high expression in the central nervous system,especially in oligodendrocytes,the physiological function of gene X in oligodendrocytes and the potential mechanisms involved in myelin formation remain unsolved.This article elaborates on the specific knockout of gene X in oligodendrocytes from the perspective of myelin development and regeneration,which seriously affects myelin formation in the central nervous system.This myelin barrier is also accompanied by impaired differentiation of oligodendrocytes.Considering that gene X is a transporter protein involved in iron transport,and iron accumulation in oligodendrocytes is necessary for their differentiation,we established a high-iron mouse model to investigate whether the role of gene X in oligodendrocytes is related to its iron transfer function.The large amount of iron supplemented in food can promote myelin formation and the differentiation process of oligodendrocytes.However,when gene X is missing,this promotion effect is significantly weakened.This result suggests that gene X may affect the differentiation of oligodendrocytes by regulating iron transport.The developmental disorders of oligodendrocytes have led to the failure of endogenous myelin regeneration in various demyelinating nervous system diseases such as multiple sclerosis(MS).Exploring the iron transport mechanism mediated by gene X may become a potential approach for treating such diseases.

研究論文（節(jié)選）

圖注:

（A-B）Ki67和Olig2在P28的f/f和f/f;Olig2小鼠胼胝體的免疫熒光染色（A）及數(shù)量統(tǒng)計結(jié)

果（B）。綠色為Ki67，紅色為Olig2，藍(lán)色為DAPI，標(biāo)尺為50μm；f/f，n=4；f/f;Olig2，

n=3，p=8.642E-05；（C-D）Olig2和CC1在P28的f/f和f/f;Olig2小鼠胼胝體的免疫熒光染色

（C）及數(shù)量統(tǒng)計結(jié)果（D）。紅色為CC1，綠色為Olig2，藍(lán)色為DAPI，標(biāo)尺為50μm；f/f，

n=6；f/f;Olig2，n=7；**p=0.0028；(E）原代細(xì)胞模型構(gòu)建流程（G）圖中所示為單細(xì)胞追蹤代表圖，原代OPC分別分離自f/f和f/f;Olig2小鼠；（H-I）總遷移路程（H）和平均運動速度（I）無差異。f/f，n=7；f/f;Olig2，n=3，總遷移路程，p=0.9140；平均速度，p=0.4288；

講解：

（A-B）共染了KI67和Olig2的抗體，并用共聚焦顯微鏡進(jìn)行拍攝，觀察到KO組小鼠胼胝體gene X缺失會引起OPC的大量增殖，細(xì)胞增殖數(shù)量遠(yuǎn)高于對照組。這表明geneX敲除導(dǎo)致的髓鞘缺失可能是因為OPC無法向成熟的少突膠質(zhì)細(xì)胞分化導(dǎo)致的

（C-D）了更好地研究geneX蛋白在少突膠質(zhì)細(xì)胞的生理功能，我們通過Cre重組酶的靶向序列l(wèi)oxp位點，制備了以Cre/loxp系統(tǒng)為依托的Olig2特異的條件性基因敲除小鼠。小鼠4周時候，我們制備了冰凍切片的樣本進(jìn)行染色觀察。結(jié)果顯示，在胼胝體區(qū)域，與WT小鼠相比，CC1標(biāo)記的成熟少突膠質(zhì)細(xì)胞數(shù)量減少，統(tǒng)計結(jié)果有統(tǒng)計顯著性，因此證明geneX的缺失會抑制少突膠質(zhì)細(xì)胞的分化。

（E）體外誘導(dǎo)分化實驗都證明缺失也會阻斷少突膠質(zhì)細(xì)胞分化。先讓原代少突膠質(zhì)質(zhì)細(xì)胞體外分離，取新生小鼠皮層培養(yǎng)成神經(jīng)干細(xì)胞（10天成球），然后用B104細(xì)胞系（大鼠神經(jīng)母細(xì)胞瘤細(xì)胞系）的上清誘導(dǎo)神經(jīng)球到少突球的轉(zhuǎn)變?nèi)缓笤侔缮偻磺蚪臃N到共聚焦皿中分化產(chǎn)生少突膠質(zhì)細(xì)胞。

(F-H）WT（野生型）和ko（基因敲除小鼠）的原代少突細(xì)胞分化不同時間點的成熟少突膠質(zhì)細(xì)胞的數(shù)量，發(fā)現(xiàn)wt組外分化一天后有成熟的MBP+（成熟細(xì)胞）體外分化三天有少量的MBP陽性的成熟細(xì)胞，分化第五天全部分化完成。而KO組在體外分化三天后才觀察到有MBP陽性的成熟細(xì)胞，分化五天只觀察到少量的成熟細(xì)胞。ko組表現(xiàn)出明顯的分化滯后性。

(A-B)Antibodies against KI67 and Olig2 were co stained and photographed using a confocal microscope.It was observed that the absence of gene X in the corpus callosum of KO group mice caused a significant proliferation of OPC,with a much higher number of cell proliferation than the control group.This suggests that the absence of myelin sheath caused by gene X knockout may be due to the inability of OPC to differentiate into mature oligodendrocytes

To better investigate the physiological function of geneX protein in oligodendrocytes,we prepared Olg2 specific conditional gene knockout mice based on the Cre/loxp system by targeting the loxp site of the Cre recombinase.At 4 weeks of age,we prepared frozen section samples for staining observation.The results showed that in the corpus callosum region,compared with WT mice,the number of mature oligodendrocytes labeled with CC1 was reduced,and the statistical results were statistically significant,indicating that the absence of geneX would inhibit the differentiation of oligodendrocytes.

(E)In vitro differentiation induction experiments have shown that deficiency can also block the differentiation of oligodendrocytes.Firstly,primary oligodendrocytes were isolated in vitro and cultured into neural stem cells(10 day old)from the cortex of newborn mice.Then,the supernatant of the B104 cell line(rat neuroblastoma cell line)was used to induce the transformation of neurons into oligodendrocytes,and then oligodendrocytes were inoculated into a confocal dish to differentiate into oligodendrocytes.

(F-H)WT(wild-type)and ko(gene knockout mice)at different time points was determined.It was found that mature MBP+(mature cells)differentiated from the WT group one day later,and a small number of MBP positive mature cells differentiated from the WT group for three days.All differentiation was completed on the fifth day.The KO group only observed mature cells with MBP positivity after three days of differentiation in vitro,and only a small number of mature cells were observed after five days of differentiation.The ko group showed significant differentiation lag.

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