Molecular characterization of unripening (ur) mutant
Ontology highlight
ABSTRACT:
ORGANISM(S): Solanum lycopersicum
PROVIDER: GSE92645 | GEO | 2018/12/01
REPOSITORIES: GEO
Similar Datasets
Project description:The tangerine2 mutant identified from Diepoxybutadiene (DEB) mutagenized population of Solanum lycopersicum and the biochemical studies revealed that mutant fruits accumulate prolycopene instead of lycopene in ripened fruits. We have developed whole genome microarray expression profiling as a discovery platform to identify differentially expressed genes in fruits tangerine2 mutant in comparison to Wild type. Tomato fruit tissue samples from different stages of fruit ripening like Mature green, Breaker, Turning and Ripening stages of tangerine2 mutant and wild type was used for microarray gene expression analysis. Carotenoid pathway analysis of both mutant and wild type reveals that the absence of expression of Carotenoid isomerase (CRTISO) gene in the tangerine2 mutant, the gene which is involved in the isomerisation of prolycopene to lycopene. Four genes (PSY, PDS, CRTISO, CYCB) of the carotenoid pathway was quantified in the same RNA samples by real-time PCR, confirming that the variation of the gene expression in Tangerine2 mutant.
2018-12-01 | GSE91045 | GEO
Project description:The High-β-Carotene (HBC) mutant identified from EMS mutagenized population of cultivar Arka Vikas and the biochemical studies revealed that mutant fruits contain four times higher level of β-Carotene in comparison to Wild type (cv. Arka Vikas). We have developed whole genome microarray expression profiling as a discovery platform to identify differentially expressed genes in fruits containing High-β-Carotene mutant in comparison to Wild type (cv. Arka Vikas). Tomato fruit tissue samples from different stages of fruit ripening like Mature green, Breaker, Turning and Ripening stages of High-β-Carotene (HBC) mutant and Wild type (cv. Arka VIkas) were used for microarray gene expression analysis. Carotenoid pathway analysis of both mutant and wild type reveals that the high expression of chromoplast specific lycopene- β-cyclase gene in the HBC mutant, which is involved in the conversion of lycopene to β-carotene, but in wild type the expression of this gene, was low. Four genes (PSY, PDS, CRTISO, CYCB) of the carotenoid pathway was quantified in the same RNA samples by real-time PCR, confirming that the variation of the gene expression in HBC mutant.
2017-12-01 | GSE90964 | GEO
Project description:An Ac/Ds transposon tagged mutant population was screened for changes in visible fruit phenotypes. One line showed orange, yellow sectors in the fruit and was named Orange ripening (Orr), its transposase free offspring showed Mendelian segregation yielding red, yellow and orange fruit bearing plants in a ratio of 1:2:1. Crossing the an orange fruit plant line to the wild-type yielded only plants bearing yellow fruit. A cross between the yellow fruit bearing progeny yielded 26 plants having red and 17 plants having yellow fruit, suggesting an over-dominant allele. Using inverse PCR analysis showed an insertion in the putative subunit M of the tomato Ndh complex. Subsequently, an Orr Ds transposon excision line was recovered which only showed red pigmented fruit. Here, we describe microarray profiling of tomato fruits from wild-type, heterozygous and homozygous Orr insertion plants and from fruits harvested from the Orr excision line. Keywords: mutant wild type Tomato fruits were harvested at breaker stage using wild-type, ORR homozygouse and heterozygous lines as well as Orr excision lines. To investigate the expression changes in the ORR mutants, wildtype and ORR mutant line fruits were harvested at the breaker stage and subjected to Affymetrix microarray profiling
2010-06-16 | E-GEOD-22110 | biostudies-arrayexpress
Project description:Gene expression in wild-type fruit. Strand-specific RNA-Seq data was used to calculate the gene expression value (RPKM) in four wild-type fruit developmental stages including immature fruit at 17DPA, mature green fruit (seeds development completes) at 39DPA, breaker fruit (onset of ripening) at 42DPA and fully ripe fruit at 52DPA. For each sample, two to four biological replicates were sequenced. Note: Samples in SRA were assigned the same sample accession. This is incorrect as there are different samples, hence âSource Nameâ was replaced with new values. Comment[ENA_SAMPLE] contains the original SRA sample accessions.
2011-10-07 | E-MTAB-4818 | biostudies-arrayexpress
Project description:The tomato MADS-box FRUITFULL (FUL) homologs, FUL1 and FUL2, interact with the main ripening regulator RIPENING INHIBITOR (RIN). To clarify their role in fruit ripening, we generated FUL1/FUL2-suppressed transgenic lines by RNAi. We found that five transgenic lines bearing fruits that did not ripen normally: lycopene accumulation and increase of ethylene production were severely inhibited. We then performed next generation RNA sequencing (RNA-Seq) analysis of the fruits of a FUL1/FUL2-suppressed line (TF18) with those of the wild type (Ailsa Craig cultivar; AC) and rin mutant. The comparison of RNA-Seq data among them indicated that FUL1/FUL2-suppression significantly affected the expression of a larger portion of ripening-induced and -repressed genes than the rin mutation did. Moreover, the effect of FUL1/FUL2-suppression was observed not only in the fruits harvested at the wild type ripening age [45 days after pollination (DAP)] but also in those at the pre-ripening age (35 DAP). This suggests that the FUL homologs play an essential role in the regulation of fruit development and ripening, the role which covers a wider range of biological processes than RIN does. Differentially expressed genes (DEGs) between the wild type and TF18 fruits included known ripening-related genes such as ACS2 and ACS4 involved in ethylene production and PSY1 in carotenoid biosynthesis, consistent with the phenotype of TF18 fruits described above. The DEGs also included many direct RIN target genes, which supports the hypothesis that the FUL homologs regulate fruit ripening in a form of MADS-box complex with RIN. mRNA profiles of wild type (Ailsa Craig cultivar), rin mutant and FUL1/FUL2-suppressed tomato fruits harvested at 35DAP and 45 DAP were generated by next generation sequencing, in triplicate, using Illumina Hiseq2000.
2014-06-23 | E-GEOD-49289 | biostudies-arrayexpress
Project description:The study of climacteric fruit ripening in tomato has been facilitated by the spontaneous ripening mutants Colorless non-ripening (Cnr), non-ripening (nor), and ripening inhibitor (rin). These mutants effect the genes encoding ripening transcription factors (TFs) SPL-CNR, NAC-NOR, and MADS-RIN causing pleiotropic defects to the ripening program. Here, we demonstrate that some ripening processes occur in the mutant fruit but at later stages of development compared to the wild type. The rin and nor mutant fruit exhibit similar quality traits to wildtype at later stages of ripening and senescence and delayed expression of ripening-associated genes. In addition, we propose that the Cnr mutant has a broader range of effects to fruit development than just fruit ripening. Cnr fruit show distinct differences from wild type in ripening phenotypic traits and gene expression profiles prior to the initiation of ripening. We provide new evidence that some mutants can produce more ethylene than basal levels and demonstrate ABA accumulation is also affected by the mutations. Studies have examined the relationship between the CNR, RIN, and NOR TFs based on protein-protein interactions and transcriptional regulation during fruit ripening. We describe the genetic interactions affecting specific fruit traits by using homozygous double mutants. Cnr predominantly influences the phenotype of the Cnr/nor and Cnr/rin double mutants but additional defects beyond either single mutation is evident in the transcriptome of the Cnr/nor double mutant. Our reevaluation of the Cnr, nor, and rin mutants provides new insights the utilization of the mutants in breeding and studying fruit development.
2020-12-24 | GSE163745 | GEO
Project description:The tomato MADS-box FRUITFULL (FUL) homologs, FUL1 and FUL2, interact with the main ripening regulator RIPENING INHIBITOR (RIN). To clarify their role in fruit ripening, we generated FUL1/FUL2-suppressed transgenic lines by RNAi. We found that five transgenic lines bearing fruits that did not ripen normally: lycopene accumulation and increase of ethylene production were severely inhibited. We then performed next generation RNA sequencing (RNA-Seq) analysis of the fruits of a FUL1/FUL2-suppressed line (TF18) with those of the wild type (Ailsa Craig cultivar; AC) and rin mutant. The comparison of RNA-Seq data among them indicated that FUL1/FUL2-suppression significantly affected the expression of a larger portion of ripening-induced and -repressed genes than the rin mutation did. Moreover, the effect of FUL1/FUL2-suppression was observed not only in the fruits harvested at the wild type ripening age [45 days after pollination (DAP)] but also in those at the pre-ripening age (35 DAP). This suggests that the FUL homologs play an essential role in the regulation of fruit development and ripening, the role which covers a wider range of biological processes than RIN does. Differentially expressed genes (DEGs) between the wild type and TF18 fruits included known ripening-related genes such as ACS2 and ACS4 involved in ethylene production and PSY1 in carotenoid biosynthesis, consistent with the phenotype of TF18 fruits described above. The DEGs also included many direct RIN target genes, which supports the hypothesis that the FUL homologs regulate fruit ripening in a form of MADS-box complex with RIN.
2014-06-23 | GSE49289 | GEO
Project description:Purpose: To identify genes regulated by SlDOF1 during fruit ripening, we performed RNAseq experiments with three biological replicates and compared the transcriptom profiles of SlDOF1-RNAi and wild-type fruit at breaker stage. Methods: Expression profiles of wild-type (wt) and SlDof1-RNAi fruits (SlDof-8-RNAi) at 38 days after poliation (dpa) were generated by deep sequencing with three replicates using Illumina HiSeqTM 2000. RNA-seq reads obtained from the replicate were further filtered and aligned against the whole tomato genome. Differential expressed genes between samples were defined by DESeq software using two separate models, based on PPEE > 0.05 and false discovery rate (FDR)<0.001. Quantitative RT–PCR was performed using SYBR Green assays. Results: A total of 1728 differentially expressed genes were identified in the SlDof1 RNAi fruit compared with the wild type and among them were a number of ripening-relate genes.
2020-12-01 | GSE119493 | GEO
Project description:Postharvest fungal pathogens benefit from the increased host susceptibility that occurs during fruit ripening. In unripe fruit, pathogens often remain quiescent and unable to cause disease until ripening begins, emerging at this point into destructive necrotrophic lifestyles that quickly result in fruit decay. Here, we demonstrate that one such pathogen, Botrytis cinerea, actively induces ripening processes in order to facilitate infections and promote disease. Assessments of ripening progression revealed that B. cinerea accelerated external coloration, ethylene production, and softening in unripe fruit, while mRNA sequencing of inoculated unripe fruit confirmed the corresponding upregulation of host genes involved in ripening processes, such as ethylene biosynthesis and cell wall degradation. Furthermore, ELISA-based glycomics profiling of fruit cell wall polysaccharides revealed remarkable similarities in the cell wall polysaccharide changes caused by both infections of unripe fruit and ripening of healthy fruit, particularly in the increased accessibility of pectin polysaccharides. Virulence and additional ripening assessment experiments with B. cinerea knockout mutants showed that induction of ripening is dependent on the ability to infect the host and break down pectin. The B. cinerea double knockout Δbcpg1Δbcpg2 lacking two critical pectin degrading enzymes was found to be incapable of emerging from quiescence even long after the fruit had ripened at its own pace, suggesting that the failure to accelerate ripening severely inhibits fungal survival on unripe fruit. These findings demonstrate that active induction of ripening in unripe tomato fruit is an important infection strategy for B. cinerea.
2022-01-01 | GSE183836 | GEO
Project description:[original title] Understanding the complexity of fruit ripening by transcriptome analysis of rin mutant fruit and in silico analysis of promoters of differentially regulated genes A tomato MADS-box transcription factor, LeMADS-RIN, controls fruit ripening and mutation in this gene results in non-ripening phenotype of fruit. This mutation down-regulates certain ripening related ethylene responses, however, other ethylene responses are normal. A complete understanding of this mutation and its effect on fruit transcriptome during ripening is not clear. In this study, microarray analysis has been used to investigate the influence of rin mutation on fruit transcriptome at different stages of ripening. A total of 2,398 genes were found to be differentially expressed in wild type fruit pericarp, which on cluster analysis indicated a major shift in their expression profiles in rin mutant fruit. A total of 1,802 genes were found to be differentially expressed between wild type and rin mutant fruits and 17% of these genes encoded regulatory elements, suggesting that mutation in LeMADS-RIN results in disturbance in the regulatory transcriptional networks during ripening. Since LeMADS-RIN has been reported to bind to the CArG box of LeACS2 promoter, in-silico analysis of 51 putative promoter sequences of the genes, that showed ripening associated up-regulation in wild type but showed impairment in up-regulation in rin mutant fruit during ripening, were searched for presence of CArG box along with ethylene and auxin responsive elements. The study revealed that only 24 putative promoter sequences harbor LeMADS-RIN specific CArG box suggesting an alternative mode of regulation by LeMADS-RIN for CArG box deficient genes.
2012-02-29 | GSE20720 | GEO