scholarly journals Regulation of Fruit Growth and Fruit Size in Apple

HortScience ◽  
2005 ◽  
Vol 40 (4) ◽  
pp. 1097A-1097
Author(s):  
Anish Malladi ◽  
Peter Goldsbrough ◽  
Peter Hirst

Fruit development in apple cultivars varying in their ultimate fruit size was analyzed using cytology, flow cytometry (FCM), and semi-quantitative RT-PCR. Fruit size variation across cultivars was largely explained by variation in cell number. The cell division phase lasted for less than 30 days in all varieties, less than previously believed. A distinct overlap between the cell division and cell expansion phases was present. Analysis of the relative cell production rate (rCPR) showed a major peak about 10 days after full bloom (DAFB) after which it declined. Comparison of the rCPR across varieties suggested distinct patterns of cell production with `Gala' having a low but sustained rCPR, `Pixy Crunch' a short but high rCPR, and `Golden Delicious' having a high and sustained rCPR. FCM analysis also showed similar patterns with a peak in the proportion of dividing cells about 10 DAFB followed by a decline. To further understand regulation of cell number, four cell cycle related genes were cloned from `Gala'. Cyclin Dependent Kinase B (CDK B) and Cyclin B were found to be highly cell division phase specific in their expression. Analysis of gene expression by semi-quantitative RT-PCR indicated peak expression of these two genes at 5-10 DAFB, consistent with the peaks in rCPR and proportion of dividing cells. Comparison of gene expression across the varieties showed higher peak expression of the above genes in the larger-fruited `Golden Delicious' than in the smaller-fruited `Gala.' This study provides novel insight into the regulation of fruit development in apple and also suggests a role for the cell cycle genes in fruit size regulation.

Plants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 585
Author(s):  
Octavio Martínez ◽  
Magda L. Arce-Rodríguez ◽  
Fernando Hernández-Godínez ◽  
Christian Escoto-Sandoval ◽  
Felipe Cervantes-Hernández ◽  
...  

Chili pepper (Capsicum spp.) is an important crop, as well as a model for fruit development studies and domestication. Here, we performed a time-course experiment to estimate standardized gene expression profiles with respect to fruit development for six domesticated and four wild chili pepper ancestors. We sampled the transcriptomes every 10 days from flowering to fruit maturity, and found that the mean standardized expression profiles for domesticated and wild accessions significantly differed. The mean standardized expression was higher and peaked earlier for domesticated vs. wild genotypes, particularly for genes involved in the cell cycle that ultimately control fruit size. We postulate that these gene expression changes are driven by selection pressures during domestication and show a robust network of cell cycle genes with a time shift in expression, which explains some of the differences between domesticated and wild phenotypes.


2011 ◽  
Vol 136 (1) ◽  
pp. 10-15 ◽  
Author(s):  
Lisa Klima Johnson ◽  
Anish Malladi ◽  
D. Scott NeSmith

Fruit size is a valuable commercial trait in blueberry. The cellular basis of variation in fruit size among rabbiteye blueberry (Vaccinium ashei) genotypes was investigated. Twenty genotypes, including cultivars and advanced selections from the University of Georgia blueberry breeding program, were analyzed. Among the 20 genotypes, fruit weight and fruit diameter varied by over threefold and 1.6-fold, respectively. Regression analysis indicated a linear relationship between fruit weight and fruit diameter (R2 = 0.97, P < 0.001), suggesting that fruit diameter is a good predictor of fruit weight. Among the 20 genotypes, mesocarp cell number and cell area varied by almost 2.5-fold and 1.5-fold, respectively. Although fruit diameter and cell number were significantly related (R2 = 0.79, P < 0.001), no relationship could be established between fruit diameter and cell area. These data indicate that variation in fruit size among rabbiteye blueberry genotypes is primarily facilitated by variation in cell number. Two small and two large fruit size genotypes were further analyzed. Differences in cell number among some of these genotypes were apparent at bloom suggesting that cell production before bloom is an important mechanism contributing to variation in final cell number. Differences in final cell number among other genotypes were manifested during fruit development, indicating that cell production during fruit development was also instrumental in determining variation in final cell number. This study suggests that fruit size variation in rabbiteye blueberry genotypes is determined by mechanisms that regulate cell production before bloom and during fruit development.


HortScience ◽  
2004 ◽  
Vol 39 (4) ◽  
pp. 868C-868
Author(s):  
Anish Malladi* ◽  
Peter Hirst

Fruit size is a commercially valuable trait. Although several factors are known to affect fruit size in apple, insights into the molecular aspects of its regulation are lacking. Our research aims to understand fruit size regulation using a combination of approaches. Analysis of a large fruited mutant of `Gala', `Grand Gala' (GG), showed that it was 40% heavier than `Gala' at harvest. Increase in size of GG fruit was caused by an increase in the cell size apparent at full bloom. Flow cytometry revealed the presence of multiple levels of ploidy (up to 16C) in GG during early fruit development. Increase in ploidy of GG is hypothesized to be due to endoreduplication, a process normally absent in apple. Endoreduplication is a modification of the cell cycle where DNA replication is not followed by cell division, resulting in increased DNA content accompanied by increased cell size. To understand if the cell cycle is altered in GG, four key cell cycle regulators, MdCDKA1, MdCDKB1, MdCYCB2 and MdCYCD3 have been partially cloned from apple using RT-PCR and RACE. As cell number at the end of the cell division phase is correlated with fruit size at harvest, expression analysis of these genes can provide valuable insights into their role in the regulation of cell number and fruit size. Analysis of cell cycle gene expression in GG may provide key insights into the altered molecular regulation that leads to endoreduplication in the mutant. Parallel approaches being employed to study whether environmental and cultural factors regulate fruit size through an influence on the cell cycle will also be discussed.


2020 ◽  
Author(s):  
Octavio Martínez ◽  
Magda L. Arce-Rodríguez ◽  
Fernando Hernández-Godínez ◽  
Christian Escoto-Sandoval ◽  
Felipe Cervantes-Hernández ◽  
...  

ABSTRACTChili pepper (Capsicum spp.) is both an important crop and a model for domestication studies. Here we performed a time course experiment to estimate standardized gene expression profiles across fruit development for six domesticated and four wild chili pepper ancestors. We sampled the transcriptome every 10 days, from flower to fruit at 60 Days After Anthesis (DAA), and found that the mean standardized expression profile for domesticated and wild accessions significantly differed. The mean standardized expression was higher and peaked earlier for domesticated vs. wild genotypes, particularly for genes involved in the cell cycle that ultimately control fruit size. We postulate that these gene expression changes are driven by selection pressures during domestication and show a robust network of cell cycle genes with a time-shift in expression which explains some of the differences between domesticated and wild phenotypes.


2004 ◽  
Vol 129 (1) ◽  
pp. 37-41 ◽  
Author(s):  
Yahya K. Al-Hinai ◽  
Teryl R. Roper

The effects of rootstock on growth of fruit cell number and size of `Gala' apple trees (Malus domestica Borkh) were investigated over three consecutive seasons (2000-02) growing on Malling 26 (M.26), Ottawa-3, Pajam-1, and Vineland (V)-605 rootstocks at the Peninsular Agricultural Research Station near Sturgeon Bay, WI. Fruit growth as a function of cell division and expansion was monitored from full bloom until harvest using scanning electron microscopy (SEM). Cell count and cell size measurements showed that rootstock had no affect on fruit growth and final size even when crop load effects were removed. Cell division ceased about 5 to 6 weeks after full bloom (WAFB) followed by cell expansion. Fruit size was positively correlated (r2 = 0.85) with cell size, suggesting that differences in fruit size were primarily a result of changes in cell size rather than cell number or intercellular space (IS).


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 966-966
Author(s):  
Stefan Nagel ◽  
Christof Burek ◽  
Hilmar Quentmeier ◽  
Corinna Meyer ◽  
Andreas Rosenwald ◽  
...  

Abstract Homeobox genes code for transcription factors with essential regulatory impact on cellular processes during embryogenesis and in the adult. Increasingly, members of the circa 200 gene strong family are emerging as major oncogenic players, prompting our investigation into possible homeobox gene dysregulation in Hodgkin lymphoma (HL) in which no recurrent oncogene involvement has been known. Accordingly, we screened 6 well characterized HL cell lines (HDLM-2, KM-H2, L-1236, L-428, L-540, SUP-HD1) and 3 non-Hodgkin lymphoma (NHL) cell lines (RC-K8, RI-1, SC-1) for homeobox gene expression using Affymetrix U133-2.0 whole-genome oligonucleotide microarrays. Of 15 candidate genes thus shown to reveal HL-specific expression patterns, 5 homeobox genes were shortlisted as potentially key dysregulatory targets in HL after additional RT-PCR expression analysis relative to controls. While 3/5 homeobox genes were upregulated in HL (HOXB9, HOXC8, HLXB9), 2/5 were downregulated (BOB1, PAX5). Furthermore, cloning and sequencing RT-PCR products obtained with degenerate primers recognizing conserved homeobox motifs confirmed the predominant expression of HOXB9 in HL cells. However, fluorescence in situ hybridization (FISH) analysis of the HOXB locus (at 17q21) revealed no cytogenetic aberrations, indicating that its activation is conducted non-chromosomally in HL cells. Surprisingly, known target genes of HOXB9 and HOXC8 remained unperturbed, implying novel downstream effector pathways in HL cells. Antisense oligos directed against HOXB9 and forced expression experiments using cloned full length HOXB9 cDNA indicated its involvement in both proliferation and apoptosis. Cell cycle regulators BTG1, BTG2 and GEMININ have been described to interact with HOXB9 and may represent potential targets deserving investigation. We recently showed that HLXB9 promotes IL6 expression in HL cells in response to a constitutively active PI3K signalling pathway therein (Nagel et al., Leukemia19, 841–6, 2005). Our most recent data indicate that HLXB9 is also expressed in various NHL cell lines including anaplastic, diffuse and mediastinal large cell as well as follicular B-cell lymphomas while expression is notably absent from Burkitt, mantle cell and natural killer T-cell lymphomas reflecting their pathologic classification. Intriguingly, our data highlight unexpected similarities between HL and prostate cancer cells which together uniquely overexpress HOXB9, HOXC8 and HLXB9 (or its close homolog GBX2). Additional genes expressed in prostate carcinoma (HOXB13, PRAC1, PRAC2) were detected in two HL cell lines (KM-H2 and L-428) suggesting further parallels may be revealed. Detection of downregulated B-cell differentiation factors BOB1 and PAX5 in our panel of HL cell lines validated this approach. Both factors were previously implicated in oncogenesis of HL lacking IGH rearrangements and other key B-cell characteristics. In summary, we identified a unique homeobox gene expression pattern involving HOXB9, HOXB13, HOXC8 and HLXB9 in HL cell lines resembling that of prostate carcinoma cells. Overexpressed HOXB9 contributes to proliferation and protects against apoptosis in HL cells potentially via interacting with cell cycle regulators BTG1/2 and/or GEMININ.


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2440-2440
Author(s):  
Chris C.S. Hsiung ◽  
Arjun Raj ◽  
Gerd A. Blobel

Abstract Normal hematopoiesis involves the coordination of cell division and gene expression to produce physiologically appropriate cell numbers of various developmental stages across lineages. While studies have demonstrated intricate links between cell cycle progression and developmental gene regulation -- two cellular programs whose concomitant dysregulation is central to many malignant and non-malignant hematologic diseases -- researchers currently lack clear, general principles of how intrinsic properties of cell division could influence developmental gene regulation. In each round of division, mitosis imposes a striking disruption to gene expression: the nucleus is disassembled, bulk RNA synthesis ceases, and the transcription machinery and most transcription factors -- including repressive complexes -- are evicted from mitotic chromatin. Since hematopoietic lineage fidelity often requires the continued presence of repressive complexes to inhibit expression of developmentally inappropriate genes, we hypothesized that such repression may be inefficient during a narrow window immediately post-mitosis, resulting in transient aberrant transcription in a probabilistic manner. We tested for the presence of transient post-mitotic aberrant transcription at genes whose repression is known to depend on continued occupancy of repressive complexes. We used an experimentally tractable cell line, G1E cells, a rapidly dividing model of lineage-committed murine pro-erythroblasts that genetically lack the erythroid master regulator Gata1. Transduction with a Gata1-estrogen receptor fusion construct and treatment with estradiol restores Gata1 function, leading to recapitulation of early erythroid maturation events, including rapid repression of stemness-associated genes, such as Gata2 and c-Kit. We examined in fine temporal detail the post-mitotic transcriptional behavior of Gata2, c-Kit and other genes using population-based assays facilitated by drug-mediated cell cycle synchronization. In addition, we bypassed the use of synchronization drugs and their associated potential experimental artifacts by developing novel complementary methods to study the relationship between cell cycle status and transcription in asynchronous populations: 1. We harnessed single-molecule RNA fluorescence in situ hybridization technology to quantitatively assess transcription in individual cells at various cell cycle stages, and 2. We adapted a fluorescent protein cell cycle reporter to separate, using fluorescence-activated cell sorting, subpopulations of specific cell cycle stages for epigenomic and transcriptomic analyses. Together, our results revealed a post-mitotic pulse of increased RNA polymerase II recruitment and transcript synthesis most clearly exhibited by Gata2, c-Kit, and other genes whose repression is known to depend on co-repressor complexes in these cells. Our results support the notion that the mitosis-G1 transition presents a window of transcriptional plasticity. We are beginning to explore how this property of post-mitotic transcriptional control applies to hematopoietic cell types across the developmental spectrum and could contribute to functionally important variations in gene expression, such as in stem cell lineage commitment, experimental reprogramming, and non-genetic heterogeneity in malignancy. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2005 ◽  
Vol 105 (2) ◽  
pp. 592-599 ◽  
Author(s):  
Marianna Kulka ◽  
Dean D. Metcalfe

Abstract T-helper 1 (TH1) (interferon-γ [IFN-γ]) and TH2 (interleukin-4 [IL-4] and IL-5) cytokines have been variably reported to alter human mast cell numbers in complex culture systems. The effects of these cytokines on the kinetics of cell division and cell death are unknown, and their effect on mast cell behavior is relevant to anticipate the consequences of in vivo strategies that alter cytokine levels. To determine the effect of these cytokines on stem cell factor (SCF)–dependent human mast cell production, we used highresolution tracking of cell division and correlated the results with cell apoptosis, expression of Kit, and mast cell degranulation. When IFN-γ, IL-5, or IL-4 was administered over 8 weeks, we found each cytokine decreased the mast number through a different mechanism. IFN-γ inhibited early progenitor cell division, IL-4 down-regulated early Kit expression, and IL-5 blocked later cell division. Further, IL-4 and IFN-γ had the greatest suppressive effect on degranulation and FcϵRI expression. When these cytokines were administered to mature mast cells, IFN-γ and IL-5 had no effect on degranulation and cell division, but IL-4 induced division and potentiated FcϵRI-mediated degranulation. Thus, exposure of human mast cells to IL-4, IL-5, and IFN-γ during growth and differentiation generally down-regulated mast cell number and function, whereas IL-4 increased mature mast cell division and degranulation.


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