Cronjé C P R, Bailey R A, Jones P, Suma S
SASA Experiment Station, P/Bag X02, Mt. Edgecombe, 4300, South Africa.
IACR-Rothamsted, Harpenden, AL52JQ, UK.
Plant Dis. 1999 Jun;83(6):588. doi: 10.1094/PDIS.1999.83.6.588A.
Ramu stunt disease of sugarcane (ScRS) was responsible for large yield losses in commercial sugarcane varieties (interspecific hybrids of Saccharum spp.) in the Ramu Valley in northeast Papua New Guinea during the late 1980s. Losses were total in the cultivar Ragnar; Q90 and Yasawa were also affected but Cadmus and Q107 were resistant. Since that time, replanting with resistant cultivars has kept the disease under control. The disease spreads rapidly in susceptible cultivars, where it results in severe stunting of the cane and a yellow mottled striping of the leaves. Although several attempts have been made to detect a viral pathogen, no evidence for viral etiology exists and the causal agent remains unknown. With a nested polymerase chain reaction (PCR) of general phytoplasma primers from the 16S rDNA (1), phytoplasma-specific products were consistently amplified from the leaves of field-grown sugarcane, from sugarcane with ScRS symptoms grown in the glasshouse at IACR-Rothamsted, UK, and from samples of the putative vector collected at Ramu, the delphacid plant hopper Eumetopina flavipes Muir, which had been found to transmit symptoms of Ramu stunt in pot trials (2). Digestion of the amplimers with restriction enzymes RsaI and HaeIII gave profiles that matched those of members of the sugarcane white leaf (SCWL) phytoplasma group. The DNA sequence of the intergenic spacer region of the phytoplasma associated with ScRS showed a 95.98% homology with that of SCWL, suggesting that this newly discovered phytoplasma can provisionally be placed in this group. The 16S-23S intergenic spacer sequence has been submitted to GenBank (accession no. AF 106061). References: (1) C. P. R. Cronjé et al. Ann. Appl. Biol. 133:177, 1998; (2) L. S. Kuniata et al. J. Aust. Entomol. Soc. 33:185, 1994.
20世纪80年代后期,甘蔗拉穆矮化病(ScRS)导致巴布亚新几内亚东北部拉穆山谷的商业甘蔗品种(甘蔗属种间杂种)大幅减产。品种Ragnar绝收;Q90和Yasawa也受到影响,但Cadmus和Q107具有抗性。自那时起,种植抗病品种使该病得到了控制。该病在易感品种中传播迅速,会导致甘蔗严重矮化以及叶片出现黄色斑驳条纹。尽管多次尝试检测病毒病原体,但没有病毒病因的证据,病原体仍然未知。利用来自16S rDNA的通用植原体引物进行巢式聚合酶链反应(PCR)(1),从田间种植的甘蔗叶片、在英国洛桑试验站温室中种植的有ScRS症状的甘蔗以及在拉穆采集的假定传毒介体样本(已发现能在盆栽试验中传播拉穆矮化症状的德尔斐叶蝉Eumetopina flavipes Muir)中,始终能扩增出植原体特异性产物。用限制性内切酶RsaI和HaeIII消化扩增产物得到的图谱与甘蔗白叶(SCWL)植原体组成员的图谱相匹配。与ScRS相关的植原体的基因间隔区DNA序列与SCWL的序列有95.98%的同源性,这表明这个新发现的植原体可以暂时归入该组。16S - 23S基因间隔序列已提交至GenBank(登录号AF 106061)。参考文献:(1)C. P. R. Cronjé等人,《应用生物学年报》133:177,1998年;(2)L. S. Kuniata等人,《澳大利亚昆虫学会杂志》33:185,1994年。