Avirulence of Magnaporthe grisea isolate CHL346 on rice cultivar GA25 was studied with 242 ascospore progenies derived from the cross CHL346

Genetic analysis and fine mapping of a resistance gene against brown planthopper (BPH) biotype 2 in rice was performed using two F2 populations derived from two crosses between a resistant indica cultivar (cv.), AS20-1, and two susceptible japonica cvs., Aichi Asahi and Lijiangxintuanheigu. Insect resistance was evaluated using F1 plants and the two F2 populations. The results showed that a single recessive gene, tentatively designated as bph19(t), conditioned the resistance in AS20-1. A linkage analysis, mainly employing microsatellite markers, was carried out in the two F2 populations through bulked segregant analysis and recessive class analysis (RCA), in combination with bioinformatics analysis (BIA). The resistance gene locus bph19(t) was finely mapped to a region of about 1.0 cM on the short arm of chromosome 3, flanked by markers RM6308 and RM3134, where one known marker RM1022, and four new markers, b1, b2, b3 and b4, developed in the present study were co-segregating with the locus. To physically map this locus, the bph19(t)-linked markers were landed on bacterial artificial chromosome or P1 artificial chromosome clones of the reference cv., Nipponbare, released by the International Rice Genome Sequencing Project. Sequence information of these clones was used to construct a physical map of the bph19(t) locus, in silico, by BIA. The bph19(t) locus was physically de-fined to an interval of about 60 kb. The detailed genetic and physical maps of the bph19(t) locus will facilitate marker-assisted gene pyramiding and cloning.

The famous rice cultivar (cv.), St. No.1, confers complete resistance to many isolates collected from the South China region. To effectively utilize the resistance, a linkage assay using microsatellite markers (SSR) was performed in the three F2 populations derived from crosses between the donor cv. St. No.1 and each of the three susceptible cvs. C101PKT, CO39 and AS20-1, which segregated into 3R:1S (resistant/susceptible) ratio, respectively. A total of 180 SSR markers selected from each chromosome equally were screened. The result showed that the two markers RM128 and RM486 located on chromosome 1 were linked to the resistance gene in the respective populations above. This result is not consistent with those previously reported, in which a well-known resistance gene Pif in the St. No.1 is located on chromosome 11. To confirm this result, additional four SSR markers, which located in the region lanked by RM128 and RM486, were tested. The results showed that markers RM543 and RM319 were closer to, and RM302 and RM212 completely co-segregated with the resistance locus detected in the present study. These results indicated that another resistance gene involved in the St. No.1, which is located on chromosome 1, and therefore tentatively designated as Pi37(t). To narrow down genomic region of the Pi37(t) locus, eight markers were newly developed in the target region through bioinformatics analysis (BIA) using the publicly available sequences. The linkage analysis with these markers showed that the Pi37(t) locus was mapped to a≈0.8 centimorgans (cM) interval flanked by RM543 and FPSM1, where a total of seven markers co-segregated with it. To physically map the locus, the Pi37(t)-linked markers were landed on the reference sequence of cv. Nipponbare through BIA. A contig map corresponding to the locus was constructed based on the reference sequence aligned by the Pi37(t)-linked markers. Consequently, the Pi37(t) locus was defined to 374 kb interval flanking markers RM543 and FPSM1, where only four candidate genes with the resistance gene conserved structure (NBS-LRR) were further identified to a DNA fragment of 60 kb in length by BIA.

Blast resistance in the indica cultivar (cv.) Q61 was inherited as a single dominant gene in two F2 populations, F2-1 and F2-2, derived from crosses between the donor cv. and two susceptible japonica cvs. Aichi Asahi and Lijiangxintuanheigu (LTH), respectively. To rapidly determine the chromosomal location of the resistance (R) gene detected in Q61, random amplified polymorphic DNA (RAPD) analysis was performed in the F2-1 population using bulked-segregant analysis (BSA) in combination with recessive-class analysis (RCA). One of the three linked markers identified, BA1126550, was cloned and sequenced. The R gene locus was roughly mapped on rice chromosome 8 by comparison of the BA1126550 sequence with rice sequences in the databases (chromosome landing). To confirm this finding, seven known markers, including four sequence-tagged-site (STS) markers and three simple-sequence repeat (SSR) markers flanking BA1126550 on chromosome 8, were subjected to linkage analysis in the two F2 populations. The locus was mapped to a 5.8cM interval bounded by RM5647 and RM8018 on the short arm of chromosome 8. This novel R gene is therefore tentatively designated as Pi36(t). For fine mapping of the Pi36(t) locus, five additional markers including one STS marker and four candidate resistance gene (CRG) markers were developed in the target region, based on the genomic sequence of the corresponding region of the reference japonica cv. Nipponbare. The Pi36(t) locus was finally localized to an interval of about 0.6cM flanked by the markers RM5647 and CRG2, and co-segregated with the markers CRG3 and CRG4. To physically map this locus, the Pi36(t)-linked markers were mapped by electronic hybridization to bacterial artificial chromosome (BAC) or P1 artificial chromosome (PAC) clones of Nipponbare, and a contig map was constructed in silico through Pairwise BLAST analysis. The Pi36(t) locus was physically delimited to an interval of about 17.0 kb, based on the genomic sequence of Nipponbare.

通过基于SRAP 标记的分子指纹分析法对由广东省40个菌株和江苏省42个菌株构成的试验群体进行了遗传结构分析。结果表明，在相似性系数取0.83 时，82个供试菌株被分为27 个宗谱；其中广东群体16 个宗谱，其宗谱频率为59.3%；江苏群体12 个宗谱，其宗谱频率为44.4%，由此说明前者比后者的遗传多样性丰富。值得指出的是，在全部27个宗谱中，只有1个宗谱是两个群体共有的，由此推测二者之间存在明显的遗传特异性。另一方面，利用中国、日本和IRRI 的三套鉴别品种分别对82个供试菌株进行了致病型结构分析。结果表明，在上述三套鉴别品种上，广东群体分别被划分为16、30 和20个小种（致病型），其小种频率分别为40.0%、75.0%和50.0%；而江苏群体则被分为8、23 和11个小种，其小种频率分别为19.0%、54.8%和26.2%。由此说明广东群体的致病型多样性也比江苏群体的丰富；在两个群体之间致病型多样性与遗传结构多样性存在相关关系。此外，对两个群体的致病型特异性和优势小种的构成进行了比较分析。结果显示，在两个群体之间存在高度的致病型特异性；优势小种的构成亦存在分明的差别。由此说明在两个群体之间致病型特异性与遗传结构特异性也是密切相关的。本研究的结果再一次说明，在进行有关病原菌群体的分子遗传学研究时，应该分别从遗传宗谱和致病型的多样性和特异性等4个方面来剖析其结构特征。