Transcriptome and Metabolome Comparison of Smooth and Rough Citrus limon L. Peels Grown on Same Trees and Harvested in Different Seasons

Background: Farmers harvest two batches fruits of Lemons (Citrus limon L. Burm. f.) i.e., spring flowering fruit and autumn flowering fruit in dry-hot valley in Yunnan, China. Regular lemons harvested in autumn have smooth skin. However, lemons harvested in spring have rough skin, which makes them less attractive to customers. Furthermore, the rough skin causes a reduction in commodity value and economical losses to farmers. This is a preliminary study that investigates the key transcriptomic and metabolomic differences in peels of lemon fruits (variety Yuning no. 1) harvested 30, 60, 90, 120, and 150 days after flowering from the same trees in different seasons.Results: We identified 5,792, 4,001, 3,148, and 5,287 differentially expressed genes (DEGs) between smooth peel (C) and rough peel (D) 60, 90, 120, and 150 days after flowering, respectively. A total of 1,193 metabolites differentially accumulated (DAM) between D and C. The DEGs and DAMs were enriched in the mitogen-activated protein kinase (MAPK) and plant hormone signaling, terpenoid biosynthesis, flavonoid, and phenylalanine biosynthesis, and ribosome pathways. Predominantly, in the early stages, phytohormonal regulation and signaling were the main driving force for changes in peel surface. Changes in the expression of genes associated with asymmetric cell division were also an important observation. The biosynthesis of terpenoids was possibly reduced in rough peels, while the exclusive expression of cell wall synthesis-related genes could be a possible reason for the thick peel of the rough-skinned lemons. Additionally, cell division, cell number, hypocotyl growth, accumulation of fatty acids, lignans and coumarins- related gene expression, and metabolite accumulation changes were major observations.Conclusion: The rough peels fruit (autumn flowering fruit) and smooth peels fruit (spring flowering fruit) matured on the same trees are possibly due to the differential regulation of asymmetric cell division, cell number regulation, and randomization of hypocotyl growth related genes and the accumulation of terpenoids, flavonoids, fatty acids, lignans, and coumarins. The preliminary results of this study are important for increasing the understanding of peel roughness in lemon and other citrus species.

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Asymmetric cell division of thoracic neuroblast 6–4 to bifurcate glial and neuronal lineage in Drosophila

Development ◽

10.1242/dev.126.9.1967 ◽

1999 ◽

Vol 126 (9) ◽

pp. 1967-1974 ◽

Cited By ~ 2

Author(s):

Y. Akiyama-Oda ◽

T. Hosoya ◽

Y. Hotta

Keyword(s):

Cell Division ◽

Glial Cells ◽

Daughter Cell ◽

Asymmetric Cell Division ◽

Cell Types ◽

Cell Number ◽

Protein Activity ◽

Neuronal Lineage ◽

Glial Fate ◽

Mother Cells

In the development of the Drosophila central nervous system, some of the neuroblasts designated as neuroglioblasts generate both glia and neurons. Little is known about how neuroglioblasts produce these different cell types. NB6-4 in the thoracic segment (NB6-4T) is a neuroglioblast, although the corresponding cell in the abdominal segment (NB6-4A) produces only glia. Here, we describe the cell divisions in the NB6-4T lineage, following changes in cell number and cell arrangement. We also examined successive changes in the expression of glial cells missing (gcm) mRNA and protein, activity of which is known to direct glial fate from the neuronal default state. The first cell division of NB6-4T occurred in the medial-lateral orientation, and was found to bifurcate the glial and neuronal lineage. After division, the medial daughter cell expressed GCM protein to produce three glial cells, while the lateral daughter cell with no GCM expression produced ganglion mother cells, secondary precursors of neurons. Although gcm mRNA was present evenly in the cytoplasm of NB6-4T before the first cell division, it became detected asymmetrically in the cell during mitosis and eventually only in the medial daughter cell. In contrast, NB6-4A showed a symmetrical distribution of gcm mRNA and GCM protein through division. Our observations suggest that mechanisms regulating gcm mRNA expression and its translation play an important role in glial and neuronal lineage bifurcation that results from asymmetric cell division.

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C. elegans Runx/CBFβ suppresses POP-1(TCF) to convert asymmetric to proliferative division of stem cell-like seam cells

10.1101/625335 ◽

2019 ◽

Author(s):

Suzanne E. M. van der Horst ◽

Janine Cravo ◽

Alison Woollard ◽

Juliane Teapal ◽

Sander van den Heuvel

Keyword(s):

Stem Cell ◽

Cell Division ◽

Asymmetric Cell Division ◽

Time Lapse ◽

Cell Number ◽

Self Renewal ◽

C Elegans ◽

Cell Divisions ◽

Seam Cell ◽

Asymmetric Divisions

ABSTRACTA correct balance between proliferative and asymmetric cell divisions underlies normal development, stem cell maintenance and tissue homeostasis. What determines whether cells undergo symmetric or asymmetric cell division is poorly understood. To gain insight in the mechanisms involved, we studied the stem cell-like seam cells in the Caenorhabditis elegans epidermis. Seam cells go through a reproducible pattern of asymmetric divisions, instructed by non-canonical Wnt/β-catenin asymmetry signaling, and symmetric divisions that increase the seam cell number. Using time-lapse fluorescence microscopy, we show that symmetric cell divisions maintain the asymmetric localization of Wnt/β-catenin pathway components. Observations based on lineage-specific knockout and GFP-tagging of endogenous pop-1 support the model that POP-1TCF induces differentiation at a high nuclear level, while low nuclear POP-1 promotes seam cell self-renewal. Before symmetric division, the transcriptional regulator rnt-1Runx and cofactor bro-1CBFβ temporarily bypass Wnt/β-catenin asymmetry by downregulating pop-1 expression. Thereby, RNT-1/BRO-1 appears to render POP-1 below the level required for its repressor function, which converts differentiation into self-renewal. Thus, opposition between the C. elegans Runx/CBFβ and TCF stem-cell regulators controls the switch between asymmetric and symmetric seam cell division.

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Roles of neuroepithelial cell rearrangement and division in shaping of the avian neural plate

Development ◽

10.1242/dev.106.3.427 ◽

1989 ◽

Vol 106 (3) ◽

pp. 427-439

Author(s):

G.C. Schoenwolf ◽

I.S. Alvarez

Keyword(s):

Cell Division ◽

Fold Increase ◽

Cell Number ◽

Neural Plate ◽

Neuroepithelial Cell ◽

Cell Rearrangement ◽

Constant Size ◽

Division Cell ◽

Longitudinal Cell ◽

Number Of Cells

Shaping of the neural plate, one of the most striking events of neurulation, involves rapid craniocaudal extension. In this study, we evaluated the roles of two processes in neural plate extension: neuroepithelial cell rearrangement and cell division. Quail epiblast plugs of constant size were grafted either just rostral to Hensen's node or paranodally and the resulting chimeras were examined at selected times postgrafting. By comparing the size of the original plug, the number of cells it contained and the distribution of cells within it to those same features of the grafts in chimeras, we were able to ascertain that, during transformation of the flat neural plate into the closed neural tube (a period requiring 24 h), the graft undergoes a maximum of 3 rounds of craniocaudal extension (each round of craniocaudal extension was defined as a doubling of graft length, so 3 rounds equaled an 8-fold increase in length). Such extension is accompanied by 2 rounds of cell rearrangement and 2–3 rounds of cell division (cell rearrangement occurred mediolaterally, so each round was defined as a halving of the number of cells in the width of the graft and a doubling of the number of cells in its length; each round of cell division was defined as a doubling of graft cell number). Modeling studies demonstrate that these amounts of cell rearrangement and division are sufficient to approximate the shaping of the neural plate that normally ensues during neurulation, provided that some of the cell division occurs within the longitudinal plane of the neural plate and some within its transverse plane: longitudinal cell division results in craniocaudal extension of the neural plate, whereas transverse cell division results in lateral expansion of the neural plate such as that occurring at its cranial end; cell rearrangement results in craniocaudal extension of the neural plate as well as in its narrowing. In conclusion, our results provide evidence that shaping of the neural plate involves mediolateral cell rearrangement and cell division, with the latter occurring within both the longitudinal and transverse planes of the neural plate.

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Centromere assembly and non-random sister chromatid segregation in stem cells

Essays in Biochemistry ◽

10.1042/ebc20190066 ◽

2020 ◽

Vol 64 (2) ◽

pp. 223-232 ◽

Cited By ~ 1

Author(s):

Ben L. Carty ◽

Elaine M. Dunleavy

Keyword(s):

Stem Cells ◽

Cell Division ◽

Cell Fate ◽

Sister Chromatid ◽

Asymmetric Cell Division ◽

Protein A ◽

Germline Stem Cells ◽

Sister Chromatids ◽

Centromere Protein A ◽

Oocyte Meiosis

Abstract Asymmetric cell division (ACD) produces daughter cells with separate distinct cell fates and is critical for the development and regulation of multicellular organisms. Epigenetic mechanisms are key players in cell fate determination. Centromeres, epigenetically specified loci defined by the presence of the histone H3-variant, centromere protein A (CENP-A), are essential for chromosome segregation at cell division. ACDs in stem cells and in oocyte meiosis have been proposed to be reliant on centromere integrity for the regulation of the non-random segregation of chromosomes. It has recently been shown that CENP-A is asymmetrically distributed between the centromeres of sister chromatids in male and female Drosophila germline stem cells (GSCs), with more CENP-A on sister chromatids to be segregated to the GSC. This imbalance in centromere strength correlates with the temporal and asymmetric assembly of the mitotic spindle and potentially orientates the cell to allow for biased sister chromatid retention in stem cells. In this essay, we discuss the recent evidence for asymmetric sister centromeres in stem cells. Thereafter, we discuss mechanistic avenues to establish this sister centromere asymmetry and how it ultimately might influence cell fate.

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