不同嫁接方法对猕猴桃成活率的影响

以野生美味猕猴桃1年生苗木作砧木,猕猴桃新品种金魁1年生枝条作接穗,进行不同嫁接方法试验。结果表明:舌接、单芽枝腹接成活率高达98.4%、96.1%,嫁接苗生长势旺,新苗基粗、新梢长度、新梢叶片数均显著高于其它几种嫁接苗。该法操作简便,是猕猴桃理想的嫁接方法,可在生产中推广应用。     

Identification of strA-strB Genes in Streptomycin-Resistant Pseudomonas syringae pv. actinidiae Biovar 2 Strains Isolated in Korea

Bacterial canker is a devastating disease of kiwifruit caused by the bacterium Pseudomonas syringe pv. actinidiae. Canker disease of kiwifruit in Korea has been controlled using streptomycin for more than two decades. Four streptomycin-resistant strains, belonging to biovar 2, which are found only in Korea, were collected between 2013 and 2014 from different orchards located in Jeju, Korea. The genetic background for streptomycin resistance among P. syringe pv. actinidiae strains were determined by examining the presence of strA-strB or aadA, which are genes frequently found in streptomycin-resistant bacteria, and a point mutation at codon 43 in the rpsL gene. All four streptomycin-resistant strains of P. syringe pv. actinidiae investigated in this study contained strA-strB as a resistant determinant. The presence of the aadA gene and a mutation in codon 43 of the rpsL gene was not identified.     

Comparative study on Pseudaulacaspis pentagona resistance of four different cultivars of kiwifruit

Kiwifruit is a common and popular fruit around the world. However, white peach scale (Pseudaulacaspis pentagona [Targioni-Tozzetti]), a scale insect with a wide range of hosts, seriously affects the yield and quality of kiwifruit. To investigate the differences in resistance of different kiwifruit cultivars to P. pentagona, cellular structure and gene expression assays were used to explain the mechanism. Based on the stability of the infestation rate, we selected four cultivars from 50 kiwifruits for in-depth study, including ‘LC-04285’, ‘CF-3’, ‘DA-7B’ and ‘Hayward’. The anatomical structure of the canes analysis revealed that the resistant cultivar ‘LC-04285’ had thicker cuticle, denser epidermis and cortex. The expression levels of genes related to cuticle synthesis and formation of epidermis and cortex were also higher in ‘LC-04285’. Further investigation revealed that Jasmonic acid (JA) receptors COI1 were highly expressed in ‘LC-04285’. However, the expression levels of AcJAZs were higher in the susceptible cultivar ‘Hayward’. Besides, AcICS, AcPAL4, AcPAL5 and AcNPRs, which were involved in salicylic acid (SA) synthesis and SA response, were also highly expressed in ‘LC-04285’. Our results preliminarily revealed the mechanism of kiwifruit resistance to P. pentagona at the molecular and cellular levels. This study provided useful guidance for breeding insect-resistant kiwifruit in the future.     

Light enhances differentiation of the vascular system in the fruit of Actinidia deliciosa

Light is recognized as crucial in determining high quality of fleshy fruits, for example, kiwifruit [Actinidia deliciosa var. deliciosa (A. Chev.) C. F. Liang et A. R. Ferguson]. Among the possible mechanisms through which light improves the quality of kiwifruit berry, there may be a direct morphogenic role on the differentiation of the fruit's vascular system, though this has not yet been investigated. The present study's aim was to determine (1) whether light positively affects the differentiation of the vascular system of the fruit and/or the pedicel, and, if so, (2) which component (xylem, phloem, or both) is more affected, and (3) in which period of the berry's development the improvement of the vascular differentiation (if any) occurs. To this end, fruit morphogenesis of kiwifruit was studied in two developmental environments (i.e., in full sunlight and in paper bags that reduced the full sunlight to 10%), and in two phases of fruit development (i.e., 1 and 5 months [harvest] after anthesis). During the growth period, the type of environment did not affect the differentiation pattern of the vascular system in the three types of bundles present in the fruit. However, in comparison with shade, light improved the vasculature in the fruit pericarp and pedicel, inducing a consistently higher extent of the xylary component in the main bundles of the fruit and pedicel, principally due to an increase in the number of xylem elements. The phloic component was also increased by light, but to a much lesser extent than that of the xylary. During the entire period of development, light-grown fruits contained higher concentrations of calcium and magnesium, as compared with shade-grown fruits. In conclusion, in the berry of Actinidia deliciosa, light enhances the differentiation of the vascular system, in particular the xylary component. The hypothesis that fruit quality is improved through a more efficient translocation of specific mineral nutrients (e.g., calcium) via the xylem is presented.     

AvrE1 and HopR1 from Pseudomonas syringae pv. actinidiae are additively required for full virulence on kiwifruit

Pseudomonas syringae pv. actinidiae ICMP 18884 biovar 3 (Psa3) produces necrotic lesions during infection of its kiwifruit host. Bacterial growth in planta and lesion formation are dependent upon a functional type III secretion system (T3S), which translocates multiple effector proteins into host cells. Associated with the T3S locus is the conserved effector locus (CEL), which has been characterized and shown to be essential for the full virulence in other P. syringae pathovars. Two effectors at the CEL, hopM1 and avrE1, as well as an avrE1-related non-CEL effector, hopR1, have been shown to be redundant in the model pathogen P. syringae pv. tomato DC3000 (Pto), a close relative of Psa. However, it is not known whether CEL-related effectors are required for Psa pathogenicity. The Psa3 allele of hopM1, and its associated chaperone, shcM, have diverged significantly from their orthologs in Pto. Furthermore, the CEL effector hopAA1-1, as well as a related non-CEL effector, hopAA1-2, have both been pseudogenized. We have shown that HopM1 does not contribute to Psa3 virulence due to a truncation in shcM, a truncation conserved in the Psa lineage, probably due to the need to evade HopM1-triggered immunity in kiwifruit. We characterized the virulence contribution of CEL and related effectors in Psa3 and found that only avrE1 and hopR1, additively, are required for in planta growth and lesion production. This is unlike the redundancy described for these effectors in Pto and indicates that these two Psa3 genes are key determinants essential for kiwifruit bacterial canker disease.