Fruit Size

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Amy F. Iezzoni - One of the best experts on this subject based on the ideXlab platform.

  • Fruit Size qtl analysis of an f1 population derived from a cross between a domesticated sweet cherry cultivar and a wild forest sweet cherry
    Tree Genetics & Genomes, 2010
    Co-Authors: Guorong Zhang, James W. Olmstead, Audrey Sebolt, S D S S Sooriyapathirana, Dechun Wang, Marco C A M Bink, Amy F. Iezzoni
    Abstract:

    Maximizing Fruit Size is critical for profitable sweet cherry (Prunus avium L.) production. Yet, despite its importance, little is known about the genetic control of Fruit Size. The objective of this study was to identify quantitative trait loci (QTLs) for Fruit Size and two essential components of Fruit Size, mesocarp cell number and Size. This study utilized a double pseudo-testcross population derived from reciprocal crosses between a sweet cherry cultivar with ~8 g Fruit, “Emperor Francis” (EF), and a wild forest sweet cherry selection with ~2 g Fruit, “New York 54” (NY). A total of 190 F1 progeny previously utilized for the construction of the linkage maps were evaluated in 2006 and 2007 for Fruit weight, length, and diameter; mesocarp cell number and length; and pit length and diameter. In 2008, a subset of this population was again evaluated for Fruit weight. Correlation analysis revealed that the three Fruit Size traits were highly correlated with each other, and mesocarp cell number, not cell length, was correlated with Fruit Size. Three QTLs were identified for each Fruit Size trait, and one QTL was identified for mesocarp cell number. Fruit Size QTLs were found on linkage group 2 on the EF map (EF 2) and linkage groups 2 and 6 on the NY map (NY 2 and NY 6). On EF 2, the cell number QTL clustered with the Fruit Size QTL, suggesting that the underlying basis of the Fruit Size increase associated with this QTL was an increase in mesocarp cell number. On NY 6, pit length and diameter QTLs clustered with those for Fruit Size, suggesting that the underlying morphological basis of this Fruit Size QTL is the difference in pit Size.

  • Genotypic Differences in Sweet Cherry Fruit Size are Primarily a Function of Cell Number
    Journal of the American Society for Horticultural Science, 2007
    Co-Authors: James W. Olmstead, Amy F. Iezzoni, Matthew D. Whiting
    Abstract:

    Understanding the genetic control of Fruit Size in sweet cherry (Prunus avium L.) is critical for maximizing Fruit Size and profitable fresh market production. In cherry, coordinated cycles of cell division and expansion of the carpel result in a fleshy mesocarp that adheres to a stony endocarp. How these structural changes are influenced by differing genetics and environments to result in differing Fruit Sizes is not known. Thus, the authors measured mesocarp cell length and cell number as components of Fruit Size. To determine the relative genotypic contribution, five sweet cherry cultivars ranging from '1 to 13 g fresh weight were evaluated. To determine the relative environmental contribution to Fruit Size, different-Size Fruit within the same genotype and from the same genotype grown in different environments were evaluated. Mesocarp cell number was the major contributor to the differences in Fruit equatorial diameter among the five sweet cherry cultivars. The cultivars fell into three significantly different cell number classes: '28 cells, '45 cells, and '78 cells per radial mesocarp section. Furthermore, mesocarp cell number was remarkably stable and virtually unaffected by the environment as neither growing location nor physiological factors that reduced final Fruit Size significantly altered the cell numbers. Cell length was also significantly different among the cultivars, but failed to contribute to the overall difference in Fruit Size. Cell length was significantly influenced by the environment, indicating that cultural practices that maximize mesocarp cell Size should be used to achieve a cultivar's Fruit Size potential. The mature cherry Fruit is composed of a thin protective exocarp, a fleshy mesocarp, and an inedible stony endocarp (pit) surrounding the seed (Esau, 1977). All three tissue types arise from the ovary, and the increase in Fruit Size results from a coordinated series of cell divisions and expansions. Fruit diameter increase in sweet cherry follows a double-sigmoid growth curve, consisting of three distinct growth stages (Coombe, 1976). Stage I is characterized by rapid and expo- nential Fruit growth following anthesis; stage II, by a lag period of Fruit growth coinciding with endocarp hardening and embryo development; and stage III, by a second period of exponential Fruit growth ending with either harvest or physiological maturity. During stage I, mesocarp growth consists of both cell division and cell enlargement, whereas stage III mesocarp growth is predominantly the result of cell expansion (Coombe, 1976; Tukey and Young, 1939). Although the growth curve for cherry is well defined, the genetic differences in cell division and enlargement contribut- ing to the wide range in Fruit Size that can occur between genotypes are not. Wild forms of forest sweet cherry have small

  • 230) Genetic Differences in Sweet Cherry Fruit Size Are Determined by Cell Number and Not Cell Size
    HortScience, 2005
    Co-Authors: James W. Olmstead, Amy F. Iezzoni, Matthew D. Whiting
    Abstract:

    Although maximizing Fruit Size is critical for profitable sweet cherry (Prunusavium L.) production, little is known about the cellular differences among and between cultivars that contribute to Fruit Size differences. A wide range of Fruit Size exists among sweet cherries, and, due to cultural and environmental differences, significant variation exists among genetically identical Fruit from the same cultivar. To determine the relative contributions of flesh cell number and cell Size to final Fruit Size in sweet cherry, equatorial sections of three cultivars with a wide range in final average Fruit Size [`New York 54' (NY54; 1.4 g fresh weight, 11.8 mm diameter), `Emperor Francis' (EF; 6.1 g, 21.0 mm), and `Selah' (12.8 g, 25.5 mm)] were created from mature Fruit. Cells intersecting a transverse line were counted and average cell length was calculated. The average cell numbers were significantly different (P ≤ 0.05) between `NY54', `EF', and `Selah' (26.7, 47.4, and 83.2, respectively), indicating that flesh cell number is the major contributor to differences in Fruit Size between cultivars. Flesh cell numbers of `NY54', `EF', and `Selah' were similar at bloom and increased rapidly for a short duration after fertilization, suggesting a key developmental period for Fruit Size differences. To determine the contribution of cell number differences to variation in Fruit Size within a cultivar, Fruit from `Bing' and `Regina' trees exhibiting a range of Size due to cultural and environmental differences were measured. In both cases, average cell number was not significantly different (P = 0.9, P = 0.3, respectively), while average cell Size was (P ≤ 0.05), further indicating Fruit flesh cell number is a genetically controlled trait.

Bin Cong - One of the best experts on this subject based on the ideXlab platform.

  • natural alleles at a tomato Fruit Size quantitative trait locus differ by heterochronic regulatory mutations
    Proceedings of the National Academy of Sciences of the United States of America, 2002
    Co-Authors: Bin Cong, Jiping Liu, Steven D Tanksley
    Abstract:

    fw2.2 is a major quantitative trait locus that accounts for as much as 30% of the difference in Fruit Size between wild and cultivated tomatoes. Evidence thus far indicates that fw2.2 alleles modulate Fruit Size through changes in gene regulation rather than in the FW2.2 protein itself. To investigate the nature of these regulatory changes and the manner in which they may affect Fruit Size, a pair of nearly isogenic lines has been subjected to detailed developmental, transcriptional, mitotic, and in situ hybridization studies. The results indicate that the large- and small-Fruited alleles of fw2.2 differ in peak transcript levels by ≈1 week. Moreover, this difference in timing of expression is associated with concomitant changes in mitotic activity in the early stage of Fruit development. The changes in timing of gene expression (heterochronic allelic variation), combined with overall differences in total transcript levels, are sufficient to account for a large portion phenotypic differences in Fruit weight associated with the two alleles.

  • fw2.2: a quantitative trait locus key to the evolution of tomato Fruit Size.
    Science (New York N.Y.), 2000
    Co-Authors: Anne Frary, T. Clint Nesbitt, Silvana Grandillo, Esther Van Der Knaap, Bin Cong, Jiping Liu, Jaroslaw Meller, Ron Elber, Kevin B. Alpert
    Abstract:

    Domestication of many plants has correlated with dramatic increases in Fruit Size. In tomato, one quantitative trait locus (QTL), fw2.2, was responsible for a large step in this process. When transformed into large-Fruited cultivars, a cosmid derived from the fw2.2 region of a small-Fruited wild species reduced Fruit Size by the predicted amount and had the gene action expected for fw2.2. The cause of the QTL effect is a single gene, ORFX, that is expressed early in floral development, controls carpel cell number, and has a sequence suggesting structural similarity to the human oncogene c-H-ras p21. Alterations in Fruit Size, imparted by fw2.2 alleles, are most likely due to changes in regulation rather than in the sequence and structure of the encoded protein.

Steven D Tanksley - One of the best experts on this subject based on the ideXlab platform.

  • natural alleles at a tomato Fruit Size quantitative trait locus differ by heterochronic regulatory mutations
    Proceedings of the National Academy of Sciences of the United States of America, 2002
    Co-Authors: Bin Cong, Jiping Liu, Steven D Tanksley
    Abstract:

    fw2.2 is a major quantitative trait locus that accounts for as much as 30% of the difference in Fruit Size between wild and cultivated tomatoes. Evidence thus far indicates that fw2.2 alleles modulate Fruit Size through changes in gene regulation rather than in the FW2.2 protein itself. To investigate the nature of these regulatory changes and the manner in which they may affect Fruit Size, a pair of nearly isogenic lines has been subjected to detailed developmental, transcriptional, mitotic, and in situ hybridization studies. The results indicate that the large- and small-Fruited alleles of fw2.2 differ in peak transcript levels by ≈1 week. Moreover, this difference in timing of expression is associated with concomitant changes in mitotic activity in the early stage of Fruit development. The changes in timing of gene expression (heterochronic allelic variation), combined with overall differences in total transcript levels, are sufficient to account for a large portion phenotypic differences in Fruit weight associated with the two alleles.

Jiping Liu - One of the best experts on this subject based on the ideXlab platform.

  • natural alleles at a tomato Fruit Size quantitative trait locus differ by heterochronic regulatory mutations
    Proceedings of the National Academy of Sciences of the United States of America, 2002
    Co-Authors: Bin Cong, Jiping Liu, Steven D Tanksley
    Abstract:

    fw2.2 is a major quantitative trait locus that accounts for as much as 30% of the difference in Fruit Size between wild and cultivated tomatoes. Evidence thus far indicates that fw2.2 alleles modulate Fruit Size through changes in gene regulation rather than in the FW2.2 protein itself. To investigate the nature of these regulatory changes and the manner in which they may affect Fruit Size, a pair of nearly isogenic lines has been subjected to detailed developmental, transcriptional, mitotic, and in situ hybridization studies. The results indicate that the large- and small-Fruited alleles of fw2.2 differ in peak transcript levels by ≈1 week. Moreover, this difference in timing of expression is associated with concomitant changes in mitotic activity in the early stage of Fruit development. The changes in timing of gene expression (heterochronic allelic variation), combined with overall differences in total transcript levels, are sufficient to account for a large portion phenotypic differences in Fruit weight associated with the two alleles.

  • fw2.2: a quantitative trait locus key to the evolution of tomato Fruit Size.
    Science (New York N.Y.), 2000
    Co-Authors: Anne Frary, T. Clint Nesbitt, Silvana Grandillo, Esther Van Der Knaap, Bin Cong, Jiping Liu, Jaroslaw Meller, Ron Elber, Kevin B. Alpert
    Abstract:

    Domestication of many plants has correlated with dramatic increases in Fruit Size. In tomato, one quantitative trait locus (QTL), fw2.2, was responsible for a large step in this process. When transformed into large-Fruited cultivars, a cosmid derived from the fw2.2 region of a small-Fruited wild species reduced Fruit Size by the predicted amount and had the gene action expected for fw2.2. The cause of the QTL effect is a single gene, ORFX, that is expressed early in floral development, controls carpel cell number, and has a sequence suggesting structural similarity to the human oncogene c-H-ras p21. Alterations in Fruit Size, imparted by fw2.2 alleles, are most likely due to changes in regulation rather than in the sequence and structure of the encoded protein.

José Antonio Campoy - One of the best experts on this subject based on the ideXlab platform.

  • Cell number regulator genes in Prunus provide candidate genes for the control of Fruit Size in sweet and sour cherry
    Molecular Breeding, 2013
    Co-Authors: P. De Franceschi, A. Cabrera, E. Van Der Knaap, T. Stegmeir, U.r. Rosyara, A.m. Sebolt, L. Dondini, Elisabeth Dirlewanger, José Quero-garcia, José Antonio Campoy
    Abstract:

    Striking increases in Fruit Size distinguish cultivated descendants from small-Fruited wild progenitors for fleshy Fruited species such as Solanum lycopersicum (tomato) and Prunus spp. (peach, cherry, plum, and apricot). The first Fruit weight gene identified as a result of domestication and selection was the tomato FW2.2 gene. Members of the FW2.2 gene family in corn (Zea mays) have been named CNR (Cell Number Regulator) and two of them exert their effect on organ Size by modulating cell number. Due to the critical roles of FW2.2/CNR genes in regulating cell number and organ Size, this family provides an excellent source of candidates for Fruit Size genes in other domesticated species, such as those found in the Prunus genus. A total of 23 FW2.2/CNR family members were identified in the peach genome, spanning the eight Prunus chromosomes. Two of these CNRs were located within confidence intervals of major quantitative trait loci (QTL) previously discovered on linkage groups 2 and 6 in sweet cherry (Prunus avium), named PavCNR12 and PavCNR20, respectively. An analysis of haplotype, sequence, segregation and association with Fruit Size strongly supports a role of PavCNR12 in the sweet cherry linkage group 2 Fruit Size QTL, and this QTL is also likely present in sour cherry (P. cerasus). The finding that the increase in fleshy Fruit Size in both tomato and cherry associated with domestication may be due to changes in members of a common ancestral gene family supports the notion that similar phenotypic changes exhibited by independently domesticated taxa may have a common genetic basis.

  • The genetic control of Fruit Size in cherry (Prunus): from phenotype to candidate genes
    2012
    Co-Authors: A. Iezzoni, A. Cabrera, P. De Franceschi, Elisa Banchi, E. Van Der Knaap, T. Stegmeir, U.r. Rosyara, A.m. Sebolt, L. Dondini, José Antonio Campoy
    Abstract:

    Sweet cherry (Prunus avium L.) is a rosaceous Fruit crop cultivated in temperate regions of the world for its highly valued Fruits. In today’s marketplace, large Fruit is highly desirable and directly related to grower profitability; therefore, the development of new cherry varieties with large Fruit is a major breeding goal. To elucidate the genetic control of Fruit Size in sweet cherry and thereby enable marker‐assisted breeding, we undertook a fine mapping – candidate gene analysis of two previously identified Fruit Size QTLs located on linkage groups 2 and 6 (G2 and G6)(Zhang et al. 2010) in two sweet cherry populations. A total of 14 simple sequence repeats were developed from the peach genomic regions syntenic to the G2 and G6 Fruit Size QTLs and used to further narrow the sweet cherry QTL regions. Genome annotations of the peach sequence in these syntenic regions identified cell number regulator genes (CNR, Guo et al. 2010) as likely candidate genes for both the G2 and G6 Fruit Size QTLs. The CNR gene family, first described in maize based upon homology to the tomato Fruit weight gene fw2.2, is hypotheSized to contain genes involved in cell number regulation that ultimately affect plant growth and organ Size. Sequencing of the CNR candidate genes from the parents of the mapping populations and a panel of diverse sweet cherry selections for G2 and G6 identified 3 and 2 allelic variants, respectively. These findings agree with the previously described functional haplotypes for these two Fruit Size QTLs. Comparisons of sweet cherry Fruit weights based on their CNR genotypes further support our hypothesis that the phenotypic differences in Fruit Size associated with the G2 and G6 QTLs are caused by allelic variants of the CNR genes.