1. Cell：揭示表觀遺傳「記憶」的傳遞機制
Title: A Tunable Mechanism Determines the Duration of theTransgenerational Small RNA Inheritance in C. elegans
Cell, 24 March 2016
Link:http://www.sciencedirect.com/science/article/pii/S0092867416302070
按照表觀遺傳學，我們的生活經歷可以傳遞給我們的孩子和孫子。但這些遺傳「記憶」究竟是如何傳遞下去的呢？來自特拉維夫大學OdedRechavi教授（http://www.sagol.tau.ac.il/en/people/dr-oded-rechavi/）領導研究小組發現小RNA分子是參與介導記憶傳遞的關鍵因子之一。在線蟲中，大多數可遺傳的表觀遺傳反應都只會持續數代。這促成了一種假設：表觀遺傳效應只會隨著時間的推移，通過一種稀釋或衰減的過程「逐漸消失」。但在該研究中，Rechavi團隊發現在線蟲中通過『開啟』和『關閉』小RNAs，操控表觀遺傳跨代持續時間的方法。基因調控的可遺傳小RNAs之間的反饋互作控制了這些開關。MOTEK基因是跨代生成和傳遞這些小RNAs的必要條件。這一反饋決定了表觀遺傳記憶是否將繼續傳給後代，以及每種表觀遺傳反應將持續的時間。
Abstract: In C.elegans, small RNAs enable transmission of epigenetic responses across multiplegenerations. While RNAi inheritance mechanisms that enable 「memorization」 ofancestral responses are being elucidated, the mechanisms that determine theduration of inherited silencing and the ability to forget the inheritedepigenetic effects are not known. We now show that exposure to dsRNA activatesa feedback loop whereby gene-specific RNAi responses dictate thetransgenerational duration of RNAi responses mounted against unrelated genes,elicited separately in previous generations. RNA-sequencing analysis revealsthat, aside from silencing of genes with complementary sequences, dsRNA-inducedRNAi affects the production of heritable endogenous small RNAs, which regulatethe expression of RNAi factors. Manipulating genes in this feedback pathwaychanges the duration of heritable silencing. Such active control oftransgenerational effects could be adaptive, since ancestral responses would bedetrimental if the environments of the progeny and the ancestors weredifferent.
2. PNAS：提升水稻抗病害能力研究取得進展
Title：ATP binding bythe P-loop NTPase OsYchF1 (an unconventional G protein) contributes to bioticbut not abiotic stress responses
PNAS, 8 March 2016
Link:http://www.pnas.org/content/113/10/2648.full.pdf
G蛋白是生物中一種常見的蛋白，但研究較少。最近來自香港中文大學的LAMHon Ming研究員（）與其合作者研究人員研究了水稻中的G蛋白，發現G蛋白在水稻中有如一個「開關掣」，可提升水稻自身的抗病害能力，以及在高鹽分土地生長的能力。一般情況下，G蛋白會與ATP或GTP結合。G蛋白與ATP結合就會減低水稻的抗病害能力，與GTP結合就會減低水稻耐鹽生長能力。研究人員利用X晶體學研究技術，拆解了G蛋白的結構，再配合定點突變技術，定點測試ATP、GTP與G蛋白的化學反應，證實ATP、GTP明顯影響水稻的抗病、對抗不良生長環境的能力。研究還發現植物特有的「OsGAP1」蛋白可以改變ATP、GTP結構，令ATP、GTP無法與G蛋白結合，G蛋白就可以啟動，令水稻自行提升抗病害及對抗不良生長環境的能力。
Abstract： G proteins are involved inalmost all aspects of the cellular regulatory pathways through their ability tobind and hydrolyze GTP. The YchF subfamily, interestingly, possesses the uniqueability to bind both ATP and GTP, and is possibly an ancestral form of Gproteins based on phylogenetic studies and is present in all kingdoms of life.However, the biological significance of such a relaxed ligand specificity haslong eluded researchers. Here, we haveelucidated the different conformational changes caused by the binding of a YchFhomolog in rice (OsYchF1) to ATP versus GTP by X-ray crystallography.Furthermore, by comparing the 3D relationships of the ligand position and thevarious amino acid residues at the binding sites in the crystal structures ofthe apo-bound and ligand-bound versions, a mechanism for the protein’s abilityto bind both ligands is revealed. Mutation of the noncanonical G4 motif of theOsYchF1 to the canonical sequence for GTP specificity precludes thebinding/hydrolysis of ATP and prevents OsYchF1 from functioning as a negativeregulator of plant-defense responses, while retaining its ability tobind/hydrolyze GTP and its function as a negative regulator of abiotic stressresponses, demonstrating the specific role of ATP-binding/hydrolysis in diseaseresistance. This discovery will have a significant impact on our understandingof the structure–function relationships of the YchF subfamily of G proteins inall kingdoms of life.
3. Plant Cell: 發現ABA信號途徑與光信號途徑互作新機制
Title: S-type Anion Channels SLAC1 and SLAH3 Function asEssential Negative Regulators of Inward K+ Channels and Stomatal Opening inArabidopsis
Plant Cell, 21 March 2016
Link: http://www.plantcell.org/content/early/2016/03/24/tpc.16.01050.abstract
乾旱脅迫和ABA信號誘導氣孔關閉，從而減少水分散失，提升植物的耐旱能力。而光照則可以誘導氣孔開放，便於植物吸收CO2和釋放氧氣，同時散失大量水分，促進植物的生長發育。但光照誘導氣孔開放必須是在沒有乾旱脅迫和ABA信號刺激的前提下才可以實現，否則光信號無法誘導氣孔開放，即乾旱/ABA信號途徑可以有效抑制光信號途徑及其誘導的氣孔開放。但多年來，乾旱信號途徑抑制光信號途徑從而進一步抑制光誘導的氣孔開放運動的信號傳遞機理並不清楚。中科院植物生理生態研究所王永飛（http://sedu.sibs.ac.cn/daoshi/2004/display.asp?ID=195）發現，乾旱誘導擬南芥氣孔保衛細胞中大量質膜慢陰離子通道（S-type anion channels）SLAC1和SLAH3的蛋白積累。SLAC1和SLAH3一方面作為質膜慢陰離子通道介導陰離子跨質膜外流，同時大量積累的SLAC1和SLAH3蛋白還通過蛋白互作的方式，強力抑制氣孔保衛細胞質膜內向K+通道，以此有效抑制光誘導的氣孔開放。眾所周知，SLAC1和SLAH3是ABA信號途徑中的關鍵組份，而質膜內向K+通道則是光信號途徑的關鍵組份。因此，該研究揭示了一個乾旱/ABA和光信號途徑互作，並共同參與氣孔運動調控的新機制。
Abstract：Drought stress induces stomatal closure and inhibits stomatalopening simultaneously. However, the underlying molecular mechanism is stilllargely unknown. Here we show that S-type anion channels SLAC1 and SLAH3 mainlyinhibit inward K+ (K+in) channel KAT1 by protein-proteininteraction, and consequently prevent stomatal opening in Arabidopsis.Voltage-clamp results demonstrated that SLAC1 inhibited KAT1 dramatically, butdid not inhibit KAT2. SLAH3 inhibited KAT1 to a weaker degree relative toSLAC1. Both the N terminus and the C terminuses of SLAC1 inhibited KAT1, butthe inhibition by the N terminus was stronger. The C terminus was essential forthe inhibition of KAT1 by SLAC1. Furthermore, drought stress stronglyup-regulated the expression of SLAC1 and SLAH3 in Arabidopsis guard cells, andthe over-expression of wild type and truncated SLAC1 dramatically impaired K+in currents of guard cells and light-induced stomatal opening. Additionally,the inhibition of KAT1 by SLAC1 and KC1 only partially overlapped, suggestingthat SLAC1 and KC1 inhibited K+in channels using different molecularmechanisms. Taken together, we discovered a novel regulatory mechanism forstomatal movement, in which singling pathways for stomatal closure and openingare directly coupled together by protein-protein interaction betweenSLAC1/SLAH3 and KAT1 in Arabidopsis.
4. Plant Cell：油菜素內酯與赤黴素兩大株高控制激素調控的關係
Title：REPLY: Brassinosteroid Regulates Gibberellin Synthesis toPromote Cell Elongation in Rice: Critical Comments on Ross and Quittenden’sLetter
Plant Cell, 22 March, 2016
Link: http://www.plantcell.org/content/early/2016/03/24/tpc.16.00123
油菜素內酯（BR）和赤黴素（GA）是兩大重要植物生長促進型激素，均顯著控制著植株高度，兩者缺失均導致植物嚴重矮化，因此，其相互調控關係一直吸引著眾多植物學家的關注。來自遺傳所的儲成才研究組(http://sourcedb.genetics.cas.cn/zw/zjrck/200907/t20090721_2130987.html)綜合已有研究成果，表明至少在擬南芥，BR和GA的互作關係基本上已完整呈現開來。BR首先通過抑制GSK3類激酶負調控子誘導BZR1轉錄因子入核並部分激活其活性來刺激GA合成，GA水平升高導致另一負調控子DELLA蛋白的降解，從而進一步激活BZR1活性調控基因表達來促進植物生長。 然而，澳大利亞的Ross和Quittenden提出了BR和GA互作的所謂「信號模型」和「合成模型」，試圖把BR和GA互作調控網絡割裂開來，認為BR與GA間的信號調控佔據主導地位，而BR對GA的合成調控相對不重要（Plant Cell, 2016)。Plant Cell在線發表的儲成才研究組和德國研究組的兩篇評論文章認為，Ross和Quittenden誤讀了多項研究數據，對相關研究結果進行過於簡單粗糙的分析。兩篇文章分別用水稻和擬南芥的研究結果對Ross he Quittenden的觀點進行了一一批駁。三篇爭鳴文章於3月22日同時在Plant Cell在線發表。
Abstract:Brassinosteroid(BR) and gibberellin (GA) are two important hormones regulating plant cellelongation. A defect in either of these hormone pathways leads to reduced plantgrowth and dwarfism. Because an early attempt in pea failed to correlate BRlevel with active GA level (Jager et al., 2005), it was presumed that BR doesnot regulate GA synthesis in plants, despite the fact that BR promotesexpression of GA biosynthetic genes in Arabidopsis (Bouquin et al., 2001; Sunet al., 2010; Lilley et al., 2013). In 2012, three studies in Arabidopsisreported the physical interaction between GA repressors DELLA proteins and BZR1in mediating BR-GA crosstalk (Bai et al., 2012; Gallego-Bartolome et al., 2012;Li et al., 2012). In Tong et al. (2014), we published results showing that BRmodulates GA levels to regulate cell elongation in rice. In our paper, wesuggest that rice may have a different mechanism from Arabidopsis as we foundthat rice BR-deficient mutants (d11-2) showed a normal response to GA, incontrast to Arabidopsis BR-deficient or insensitive mutants (det2-1, bri1-5,and bri1-119) that were reported to be insensitive to GA application at earlyseedling stages (Bai et al., 2012). Unterholzner et al. (2015) subsequentlyreported similar results in Arabidopsis, confirming our finding in rice that BRpromotes GA biosynthesis to regulate plant growth. They also showed thatBR-deficient mutants (cpd, bri1-1, and bri1-301) have normal responses to GA atdifferent growth stages. Integrating all of these results, Unterholzner et al.(2015) proposed an updated model for BR-GA crosstalk: BR promotes BZR1/BES1 toinduce GA biosynthesis and the increased GA level promotes DELLA degradation tofurther release BZR1/BES1 activity.
5. PloS Genetics：發現水稻開花調節因子
Title: The Oryza sativaRegulator HDR1 Associates with the Kinase OsK4 to Control PhotoperiodicFlowering
Plos Genetics, 8 March, 2016
Link: http://journals.plos.org/plosgenetics/article?id=10.1371%2Fjournal.pgen.1005927
水稻是一種兼性短日植物，開花時間的調控途徑在擬南芥和水稻中是保守的，但是可在功能上進行修飾。Hd1是擬南芥CONSTANS (CO)的一個同源基因，是在長日照條件下抑制開花的一個關鍵調節因子，但是可在短日照條件下，通過影響成花素基因Hd3a的表達，促進開花。另一個關鍵的調節因子Ehd1是一個進化上獨特的基因，在擬南芥中沒有同源基因，短日照和長日照條件下，可促進水稻成花素基因Hd3a和RFT1，是一個開花激活因子。來自農科院的生物技術研究所的路鐵剛研究組（http://bri.caas.net.cn/rcdw/in_04.aspx?id=30）在水稻中分離和鑑定了開花調節因子HDR1。hdr1突變體在北京稻田的自然長日照條件、以及在溫室的長日照條件（而不是短日照）下，表現出早期開花的表型，從而表明HDR1可能通過光周期依賴性途徑，功能性地調節開花時間。HDR1編碼一個核蛋白，該蛋白在葉片和花器官中最為活躍，並表現出一種典型的晝夜表達模式。研究人員認為，HDR1是一種新的開花抑制因子，可上調Hd1，下調Ehd1，從而導致長日照條件下Hd3a和RFT1的下調。研究人員進一步確定了一個HDR1相互作用激酶——OsK4，在長日照條件下水稻開花的另一個抑制因子。OsK4的作用跟HDR1相同，在長日照條件下通過上調Hd1和下調Ehd1，抑制開花。這些結果指出，轉錄調節因子Hd1，可依賴於光日照長度，控制水稻的開花時間。
Abstract:Rice is afacultative short-day plant (SDP), and the regulatory pathways for floweringtime are conserved, but functionally modified, in Arabidopsis and rice. Headingdate 1 (Hd1), an ortholog of ArabidopsisCONSTANS (CO), is a key regulatorthat suppresses flowering under long-day conditions (LDs), but promotesflowering under short-day conditions (SDs) by influencing the expression of theflorigen gene Heading date 3a (Hd3a).Another key regulator, Early heading date 1 (Ehd1),is an evolutionarily unique gene with no orthologs inArabidopsis, which acts asa flowering activator under both SD and LD by promoting the rice florigen genes Hd3a and RICE FLOWERING LOCUST 1 (RFT1).Here, we report the isolation and characterization of the flowering regulator Heading Date Repressor1(HDR1) in rice. The hdr1 mutant exhibits an early floweringphenotype under natural LD in a paddy field in Beijing, China (39°54'N,116°23'E), as well as under LD but not SD in a growth chamber, indicating that HDR1 may functionally regulate floweringtime via thephotoperiod-dependent pathway. HDR1 encodes a nuclear protein that is mostactive in leaves and floral organs and exhibits a typical diurnal expressionpattern. We determined that HDR1 is a novel suppressor of flowering thatupregulates Hd1 and downregulates Ehd1,leading to the downregulation of Hd3a and RFT1 under LDs. We have further identifiedan HDR1-interacting kinase, OsK4, another suppressor of rice flowering underLDs. OsK4 actssimilarly to HDR1, suppressingflowering by upregulating Hd1 and downregulating Ehd1underLDs, and OsK4 can phosphorylate HD1 with HDR1 presents. These resultscollectively reveal the transcriptional regulators of Hd1 for the day-length-dependent controlof flowering time in rice.
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