公司绩效考核办法附全套表格及操作方案

1、Mol Genet Genomics (2008 279:605619615defense genes than leaves above or below, even in thewild-type plant (IR64 for several genes.Expression patterns of PR-10a were generally correlatedwith strength of lesion appearance in all of the lines, withthe exception of leaf 2, as noted above, where relativ

2、elyhigh levels of expression were observed even with nolesions in IR64 and spl 6-2. Elevated POX22.3 expressionwas observed earlier and/or to a higher degree in the singlemutants than in the wild type, but was particularly higher inthe double mutant relative to the single mutants. No expres-sion of

3、PO-C1 was evident in wild-type IR64 and spl 6-2but a moderate level of expression was observed in spl 17(leaf 2 and spl 6-2/spl17 (leaf 23. Similar to POX22.3, PO-C1 was expressed strongly in the two youngest leavesof Spl 26. PR1 expression was detectable in the older leavesof Spl 26, but had little

4、 or no expression in the wild type andthe other mutants.Overall, the levels of expression of PR-10a , POX22.3, and PO-C1 in spl 17 and the double mutant spl 6-2/spl17were correlated with lesion density and disease reaction,whereas PR-1 expression was not correlated with thesephenotypes. However, whe

5、reas PR-10a expression wassustained in the oldest leaves (leaf 4, expression ofPOX22.3 was attenuated in the older leaves, suggestingthat downstream regulation of these genes is diV erent. Elevated levels of expression of PR10a , POX22.3, andPO-C1 were observed in Spl 26, similar to that in spl 6-2/

6、s pl 17, but the timing diV ered in the two genotypes, asindicated by sampling diV erent leaf positions. The mostdistinct diV erence was observed in PR-1 which wasexpressed in Spl 26 starting from leaf 2 but not in spl 6-2/spl 17, suggesting that the resistance observed in diV erent lesion mimic mut

7、ants is moderated by diV erent molecularmechanisms.cantly diV erent at P >0.5 based on comparison of least square means.123616123Mol Genet Genomics (2008 279:605619DiscussionLesion mimics represent a broad phenotypic class encom-passing all mutations causing spontaneous cell death. Thetime and co

8、nditions of lesion appearance, and color andsize of lesions are diV erent in these mutants. Diverse struc-ture of the cloned lesion mimic genes suggests that lesionmimics are caused by genes involved in diV erent biologicalprocesses (Lorrain etal. 2003. In this study, we recovered70 lesion mimic mut

9、ations from a screen of over 11,000mutant lines, giving a frequency of 0.6%. The relativelyhigh frequency of this mutant class suggests that manymutations could lead to cell death. In maize, it has beenestimated that there are more than 200 lesion mimic genes(Johal etal. 1995; Walbot 1991. In rice,

10、many lesionmimic mutants have been reported, but the allelic relation-ships of these mutations were not well deW ned. We havede W ned the allelic relationship of 21 lesion mimic mutantsof IR64 with nine known spotted leaf mutants. We foundW ve mutations, which were allelic with these known muta-tion

11、s, and 11 new mutations.Although not all mutated genes leading to lesion mimicsare necessarily involved in defense pathways, many lesionmimic mutants exhibit broad-spectrum resistance makingthem a useful vehicle to identify candidate genes conferringresistance to multiple diseases. For example, a ma

12、jority ofthe 37 lesion mimic mutants identiW ed in Arabidopsis showed enhanced resistance to one or more pathogens(Lorrain etal. 2003. Several cloned genes have beenplaced in the resistance-signaling pathways through geneticand mutation analysis. We found a majority of the lesionmimic mutants showin

13、g resistance to multiple races of thebacterial blight pathogen. Four of the lesion mimic mutantsshowed resistance to blast. Takahashi etal. (1999 foundthat only a small proportion of the 93 lesion mimic mutantsscreened exhibited enhanced resistance to M. oryzae. Thiscould be due to the inoculation w

14、ith diV erent pathogens atdi V erent plant developmental stages. Also, it could beattributed to the advantage of comparing all mutations in acommon IR64 background, allowing more accurate mea-surement of the quantitative diV erences between mutants(Mizobuchi etal. 2002a .Many mutations (e.g. spl 23,

15、 Spl 24 are only marginallymore bacterial blight resistant than the wild type. OnlySpl 26 showed a level of resistance as strong as that con-ferred by major Xa resistance genes. The resistance to bac-terial blight that we observed in several lesion mimics is notrace-speci W c; suggesting that the de

16、fense mechanisms arelikely downstream of the recognition steps mediated bymajor resistance genes. Previous reports on spl 11 (Yin etal. 2000 and several other lesion mimic mutants (MizobuchiMol Genet Genomics (2008 279:605619et al. 2002a suggest that the lesion mimic mutations conferresistance to mu

17、ltiple diseases. Although we have nottested all the mutants against multiple diseases, two of thebacterial blight resistant mutants, spl 17 and Spl 26, werefound to be partially resistant to M. oryzae. Preliminaryresults also suggest that spl 17 is resistant to brown spotcaused by Cochliobolus miyab

18、eanus (S. Madamba etal., unpublished data, IRRI and to sheath blight caused by Rhi-zoctonia solani (G. Saludares and C. Vera Cruz, unpub-lished data, IRRI. Work is in progress to test whether theresistance observed in these lesion mimics mutants is eV ec-tive against diV erent pathogens.The lesion m

19、imic phenotypes provide a convenientmarker system to investigate the epistatic interactionsbetween the lesion mimic mutations and their phenotypice V ects. Mutations in genes that act in parallel or redundantpathways should exhibit an additive or synergistic pheno-type when combined. On the other ha

20、nd, lethality may alsoresult if the two mutations together impose a severe W tness penalty. Indeed, out of 109 attempted crosses, 14 (13%produced inviable or sub-lethal double mutants (A. Bordeosand H. Leung, unpublished data, IRRI. We produced adouble mutant between spl 6-2 and spl 17 as a W rst st

21、ep togroup lesion mimic mutations. The co-appearance of lesiontypes in the double mutant suggests that the individualgenes act independently in distinct pathways, giving rise tocharacteristic lesion types. However, it is possible, thoughless likely, that two weak mutations are located in the samepat

22、hway and that their double mutants could show additivee V ects of the single mutations (Martienssen and Irish 1999. While spl 6-2 did not show signiW cant disease resistanceenhancement, the double mutant spl 6-2/spl 17 showed amuch stronger expression of lesion mimic that corre-sponded to a higher l

23、evel of resistance. This result suggeststhat the two mutations aV ect independent pathways. Bytriggering diV erent defense pathways, the plant becomesmore restrictive to pathogen ingress or growth; however,there is a clear penalty due to an increase in severity oflesion mimics. Exactly as to where t

24、hese pathways con-verge is not clear. The expression data from the fewdefense gene markers we used here do not help answeringthis question as none of the genes were uniquely expressedin a given mutant (when intensity of lesions on a givenmutant are taken into account. However, the elevatedexpression

25、 of POX22.3 and PO-C1 in the BB-resistantmutants spl 17, Spl 26, and the double mutant spl 6-2/spl 17 isconsistent with the hypothesis that the mutations aV ect genes involved in defense response.In conclusion, we have identiW ed new independentlesion mimic mutations, expanding the pool of mutantres

26、ources available for investigating pathways involved indisease resistance and cell death. The isogenic backgroundof these mutants will facilitate phenotypic and molecular617characterization. Having mutations in an identical geneticbackground will allow the production of double mutantsmore amenable f

27、or comparative analyses. We have so farcreated 74 additional double lesion mimic mutants to deter-mine the relationship of downstream or upstream genes toimprove our understanding on the rice resistance pathways(A. Bordeos, unpublished data, IRRI. Our next step is touse genome-wide oligo chips to pr

28、oW le these mutants sothat the mutations can be grouped into diV erent biochemi-cal pathways.Acknowledgments We thank the technical help of Pedro Reaño,Alexander Ramos, and Benedicto Consignado. We also thank VioletaBartolome for assistance in statistical analyses. The work was sup-ported in pa

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