Role of Changes in Cell Size in the Evolution of Wheat

1974 ◽  
Vol 1 (1) ◽  
pp. 157 ◽  
Author(s):  
RL Dunstone ◽  
LT Evans

The objective of the present work was to examine to what extent increase in cell size has contributed to the parallel increases in leaf and grain size in the course of evolution in wheat. Eighteen lines were chosen to represent wild and cultivated wheats at the diploid and tetraploid levels, cultivated hexaploid wheats, and the two Aegilops species likely to have contributed the B and D genomes. All plants were grown at 21/16�C under natural light. The penultimate leaves and the basal grains from central spikelets were selected for comparison. The projected area of separated mesophyll cells from leaves was 1.5–2 times larger in the cultivated tetraploid and hexaploid wheats than in the diploids, and correlated positively but weakly with leaf blade area (r = 0.50), and negatively with photosynthetic rate in Triticum species (r = -0.66). Cell size in the endosperm bore no relation to cell size in the aleurone layer or mesophyll, or to grain volume. Aleurone cell size, however, correlated positively with both grain volume (r = 0.82) and mesophyll cell size (r = 0.79). Increase in grain weight during evolution has not involved increase in either specific gravity of the mature grain or endosperm cell size. Presumably increase in endosperm cell number has been the major factor. With increase in grain size during evolution there has been a fall in percentage nitrogen in the grain.

2021 ◽  
Author(s):  
Zhijie Ren ◽  
Fenglin Bai ◽  
Jingwen Xu ◽  
Li Wang ◽  
Xiaohan Wang ◽  
...  

SummaryGrain size is determined by the number of cells and cell size of the grain. Regulation of grain size is crucial for improving crop yield. However, the genes and underlying molecular mechanisms controlling grain size remain elusive. Here we report a member of Detoxification efflux carrier (DTX)/Multidrug and Toxic Compound Extrusion (MATE) family transporter, BIG RICE GRAIN 1 (BIRG1), negatively regulates the grain size in rice. BIRG1 is highly expressed in reproductive organs and roots. In birg1 grain, the size of the outer parenchyma layer cells of spikelet hulls is noticeably larger but the cell number is not altered compared with that in the wild-type (WT) grain. When expressed in Xenopus oocytes, BIRG1 exhibits chloride efflux activity. In line with the role of BIRG1 in mediating chloride efflux, the birg1 mutant shows reduced tolerance to salt stress under which the chloride level is toxic. Moreover, the birg1 grains contain higher level of chloride compared to WT grains when grown under normal paddy field. The birg1 roots accumulate more chloride than those of WT under saline condition. Collectively, our findings suggest that BIRG1 functions as a chloride efflux transporter regulating grain size and salt tolerance via controlling chloride homeostasis in rice.


Planta ◽  
2019 ◽  
Vol 251 (1) ◽  
Author(s):  
D. Santeramo ◽  
J. Howell ◽  
Y. Ji ◽  
W. Yu ◽  
W. Liu ◽  
...  

Abstract Main conclusion The qPCR assay developed to differentiate haploid and diploid maize leaf samples was unsuccessful due to DNA content difference. Haploid cells are packed more closely together with less cellular expansion. Abstract Increased ploidy content (> 2 N) directly correlates with increased cell size in plants, but few studies have examined cell morphology in plants with reduced ploidy (i.e., haploids). To pioneer a scalable new ploidy test, we compared DNA content and cellular morphology of haploid and diploid maize leaves. The amount of genomic DNA recovered from standardized leaf-punch samples was equivalent between these two ploidy types, while both epidermal and mesophyll cell types were smaller in haploid plants. Pavement cells had a substantially smaller size than mesophyll cells, and this effect was more pronounced in the abaxial epidermis. Interveinal distance and guard cell size were significantly reduced in haploids, but the cell percentage comprising stomata did not change. These results confirm the direct correlation between ploidy content and cell size in plants, and suggest that reduced cell expansion predominantly explains DNA content equivalence between haploid and diploid samples, confounding efforts to develop a haploid detection method using DNA content.


2018 ◽  
Author(s):  
Douaa Mugahid ◽  
Marian Kalocsay ◽  
Scott Gruver ◽  
Leonid Peshkin ◽  
Marc W. Kirschner

SummaryThe Hippo pathway, in which changes at the cell surface and in the extracellular environment control the activity of a downstream transcription factor, known as YAP in mammalian cells and Yorkie in Drosophila, has recently taken center-stage as perhaps the most important pathway in metazoans for controlling organ size. In intact tissues YAP activity is inhibited and the organ does not overgrow. When the organ is damaged, YAP is active and necessary for growth and regeneration to occur. The exact process by which YAP drives organ and tissue growth is not fully understood, although it is known to affect both cell size and cell number. Since cell size and proliferation are highly interdependent in many cultured cell studies, we investigated the role of YAP in the simultaneous regulation of both cell size and number. Our experiments reveal that YAP controls both cell size and cell proliferation by independent circuits, and that it affects each process non-cell autonomously via extracellular mediators. We identify that CYR61, a known secreted YAP target, is the major regulator of the non-cell autonomous increase in cell number, but does not affect cell size. The molecular identity of the non-cell autonomously acting mediator of cell size is yet to be identified.


‘Growth of tissues and organs’ is an overview of the general principles of tissue growth due to changes in cell size (normal and pathological atrophy, hypertrophy including pathological conditions) or cell number (hyperplasia). Neoplasia, the formation of neoplasms (i.e. cancerous tumours), is considered, including naming conventions for neoplasms, their morphology, and molecular mechanisms of formation and growth, including gains in gene function (proto-oncogenes, such as p53 and adenomatous polyposis coli) and environmental carcinogens, and the role of metastasis in disease progression. Finally, their treatment by chemotherapy and radiobiology is discussed.


Genetics ◽  
2001 ◽  
Vol 159 (2) ◽  
pp. 787-797
Author(s):  
Lizzie Cribb ◽  
Lisa N Hall ◽  
Jane A Langdale

Abstract Maize leaf blades differentiate dimorphic photosynthetic cell types, the bundle sheath and mesophyll, between which the reactions of C4 photosynthesis are partitioned. Leaf-like organs of maize such as husk leaves, however, develop a C3 pattern of differentiation whereby ribulose bisphosphate carboxylase (RuBPCase) accumulates in all photosynthetic cell types. The Golden2 (G2) gene has previously been shown to play a role in bundle sheath cell differentiation in C4 leaf blades and to play a less well-defined role in C3 maize tissues. To further analyze G2 gene function in maize, four g2 mutations have been characterized. Three of these mutations were induced by the transposable element Spm. In g2-bsd1-m1 and g2-bsd1-s1, the element is inserted in the second intron and in g2-pg14 the element is inserted in the promoter. In the fourth case, g2-R, four amino acid changes and premature polyadenylation of the G2 transcript are observed. The phenotypes conditioned by these four mutations demonstrate that the primary role of G2 in C4 leaf blades is to promote bundle sheath cell chloroplast development. C4 photosynthetic enzymes can accumulate in both bundle sheath and mesophyll cells in the absence of G2. In C3 tissue, however, G2 influences both chloroplast differentiation and photosynthetic enzyme accumulation patterns. On the basis of the phenotypic data obtained, a model that postulates how G2 acts to facilitate C4 and C3 patterns of tissue development is proposed.


2021 ◽  
Vol 22 (4) ◽  
pp. 1707
Author(s):  
Sebastian Granitzer ◽  
Raimund Widhalm ◽  
Martin Forsthuber ◽  
Isabella Ellinger ◽  
Gernot Desoye ◽  
...  

The placental barrier can protect the fetus from contact with harmful substances. The potent neurotoxin methylmercury (MeHg), however, is very efficiently transported across the placenta. Our previous data suggested that L-type amino acid transporter (LAT)1 is involved in placental MeHg uptake, accepting MeHg-L-cysteine conjugates as substrate due to structural similarity to methionine. The aim of the present study was to investigate the antioxidant defense of placental cells to MeHg exposure and the role of LAT1 in this response. When trophoblast-derived HTR-8/SVneo cells were LAT1 depleted by siRNA-mediated knockdown, they accumulated less MeHg. However, they were more susceptible to MeHg-induced toxicity. This was evidenced in decreased cell viability at a usually noncytotoxic concentration of 0.03 µM MeHg (~6 µg/L). Treatment with ≥0.3 µM MeHg increased cytotoxicity, apoptosis rate, and oxidative stress of HTR-8/SVneo cells. These effects were enhanced under LAT1 knockdown. Reduced cell number was seen when MeHg-exposed cells were cultured in medium low in cysteine, a constituent of the tripeptide glutathione (GSH). Because LAT1-deficient HTR-8/SVneo cells have lower GSH levels than control cells (independent of MeHg treatment), we conclude that LAT1 is essential for de novo synthesis of GSH, required to counteract oxidative stress. Genetic predisposition to decreased LAT1 function combined with MeHg exposure could increase the risk of placental damage.


Diabetologia ◽  
2021 ◽  
Author(s):  
Hironobu Sasaki ◽  
Yoshifumi Saisho ◽  
Jun Inaishi ◽  
Yuusuke Watanabe ◽  
Tami Tsuchiya ◽  
...  

Abstract Aims/hypothesis Type 2 diabetes is characterised by reduced beta cell mass (BCM). However, it remains uncertain whether the reduction in BCM in type 2 diabetes is due to a decrease in size or number of beta cells. Our aim was to examine the impact of beta cell size and number on islet morphology in humans with and without type 2 diabetes. Methods Pancreas samples were obtained from 64 Japanese adults with (n = 26) and without (n = 38) type 2 diabetes who underwent pancreatectomy. Using pancreatic tissues stained for insulin, we estimated beta cell size based on beta cell diameter. Beta cell number was estimated from the product of fractional beta cell area and pancreas volume divided by beta cell size. The associations of beta cell size and number with islet morphology and metabolic status were examined. Results Both beta cell size (548.7 ± 58.5 vs 606.7 ± 65.0 μm3, p < 0.01) and number (5.10 × 108 ± 2.35 × 108 vs 8.16 × 108 ± 4.27 × 108, p < 0.01) were decreased in participants with type 2 diabetes compared with those without diabetes, with the relative reduction in beta cell number (37%) being greater than for beta cell size (10%). Beta cell number but not size was positively correlated with BCM in participants with and without type 2 diabetes (r = 0.97 and r = 0.98, both p < 0.01) and negatively correlated with HbA1c (r = −0.45, p < 0.01). Conclusions/interpretation Both beta cell size and number were reduced in participants with type 2 diabetes, with the relative reduction in beta cell number being greater. Decrease in beta cell number appears to be a major contributor to reduced BCM in type 2 diabetes. Graphical abstract


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