Comparative transcriptome analyses shed light on carotenoid production and plastid development in melon fruit

Carotenoids,such asβ-carotene,accumulate in chromoplasts of various fleshy fruits,awarding them with colors,aromas,and nutrients.The Orange(CmOr)gene controlsβ-carotene accumulation in melon fruit by posttranslationally enhancing carotenogenesis and repressingβ-carotene turnover in chromoplasts.Carotenoid isomerase(CRTISO)isomerizes yellow prolycopene into red lycopene,a prerequisite for further metabolism intoβ-carotene.We comparatively analyzed the developing fruit transcriptomes of orange-colored melon and its two isogenic EMS-induced mutants,low-β(Cmor)and yofi(Cmcrtiso).The Cmor mutation in low-βcaused a major transcriptomic change in the mature fruit.In contrast,the Cmcrtiso mutation in yofi significantly changed the transcriptome only in early fruit developmental stages.These findings indicate that melon fruit transcriptome is primarily altered by changes in carotenoid metabolic flux and plastid conversion,but minimally by carotenoid composition in the ripe fruit.Clustering of the differentially expressed genes into functional groups revealed an association between fruit carotenoid metabolic flux with the maintenance of the photosynthetic apparatus in fruit chloroplasts.Moreover,large numbers of thylakoid localized photosynthetic genes were differentially expressed in low-β.CmOR family proteins were found to physically interact with light-harvesting chlorophyll a–b binding proteins,suggesting a new role of CmOR for chloroplast maintenance in melon fruit.This study brings more insights into the cellular and metabolic processes associated with fruit carotenoid accumulation in melon fruit and reveals a new maintenance mechanism of the photosynthetic apparatus for plastid development.

Localization of the Arabidopsis Senescence- and Cell Death-Associated BFN1 Nuclease： From the ER to Fragmented Nuclei

Plant senescence- or PCD-associated nucleases share significant homology with nucleases from different organisms. However, knowledge of their function is limited. Intracellular localization of the Arabidopsis senescence- and PCD-associated nuclease BFN1 was investigated. Analysis of BFN1-GFP localization in transiently transformed tobacco protoplasts revealed initial localization in filamentous structures spread throughout the cytoplasm, which then clustered around the nuclei as the protoplasts senesced. These filamentous structures were identified as being of ER origin. In BFN1- GFP-transgenicArabidopsis plants, similar localization of BFN1-GFP was observed in young leaves, that is, in filamentous structures that reorganized around the nuclei only in senescing cells. In late senescence, BFN1-GFP was localized with fragmented nuclei in membrane-wrapped vesicles. BFNI＇s postulated function as a nucleic acid-degrading enzyme in senescence and PCD is supported by its localization pattern. Our results suggest the existence of a dedicated compartment mediating nucleic acid degradation in senescence and PCD processes.

Dual Resistance of Melon to Fusarium oxysporum Races 0 and 2 and to Papaya ring-spot virus is Controlled by a Pair of Head-to-Head-Oriented NB-LRR Genes of Unusual Architecture

Dear Editor, Potyviruses such as Papaya ring-spot virus （PRSV） cause important yield losses in cucurbits. Two distinct resistant alleles were identified in the Cucumis melo germplasm. Accession PI 414723 （Supplemental Table 1） possesses mono- genic resistance, controlled by the Prv2 allele, and reacts to PRSV by systemic necrotic lesions; plants with the PryI allele, described in cultivar WMR-29, remain symptomless （Pitrat and Lecoq, 1983）. Fusarium oxysporum f. sp. melonis （FUS） exclusively attacks melon, causing severe wilt. Monogenic dominant resistance was described against races O, 1, and 2. The Fore-2 gene, controlling resistance to races 0 and 1, was cloned by Joobeur et al. （2004）, and encodes a nucleotide bindina domain （NB）-Ieucine rich repeat （LRR） protein.