scholarly journals Cells from the same lineage switch from reduction to enhancement of size variability in Arabidopsis sepals

2017 ◽  
Author(s):  
Satoru Tsugawa ◽  
Nathan Hervieux ◽  
Daniel Kierzkowski ◽  
Anne-Lise Routier-Kierzkoswska ◽  
Aleksandra Sapala ◽  
...  

AbstractOrgans form with remarkably consistent sizes and shapes during development, whereas a high variability in size and growth is observed at cell level. Given this contrast, it is unclear how such consistency at organ scale can emerge from cellular behavior. We examine the growth of cell lineages, or groups of cells that are the progeny of a single mother cell. At early stages of the lineage, we find that initially smaller lineages grow faster than the larger ones reducing variability in lineage size, a phenomenon we refer to as size uniformization. In contrast at later stages of the lineage, size variability is enhanced when initially larger cell lineages grow faster than the smaller ones. Our results imply that the cell lineage changes its growth pattern at a tipping point. Finally, we found that the growth heterogeneity of individual cells within a lineage is correlated with fast growth of the lineage. Consequently, fast growing lineages show greater cell growth heterogeneity, leading to uniformization in lineage size. Thus, cellular variability in growth contributes toward decreasing variability of cell lineages throughout the sepal.

1998 ◽  
Vol 353 (1370) ◽  
pp. 925-933 ◽  
Author(s):  
Nicholas A. Wright

The main pathways of epithelial differentiation in the intestine, Paneth, mucous, endocrine and columnar cell lineages are well recognized. However, in abnormal circumstances, for example in mucosal ulceration, a cell lineage with features distinct from these emerges, which has often been dismissed in the past as ‘pyloric’ metaplasia, because of its morphological resemblance to the pyloric mucosa in the stomach. However, we can conclude that this cell lineage has a defined phenotype unique in gastrointestinal epithelia, has a histogenesis that resembles that of Brunner's glands, but acquires a proliferative organization similar to that of the gastric gland. It expresses several peptides of particular interest, including epidermal growth factor, the trefoil peptides TFF1, TFF2, TFF3, lysozyme and PSTI. The presence of this lineage also appears to cause altered gene expression in adjacent indigenous cell lineages. We propose that this cell lineage is induced in gastrointestinal stem cells as a result of chronic mucosal ulceration, and plays an important part in ulcer healing; it should therefore be added to the repertoire of gastrointestinal stem cells.


Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 435-454 ◽  
Author(s):  
H Robert Horvitz ◽  
John E Sulston

ABSTRACT Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized. In some of these mutants, cell divisions fail that occur in wild-type animals; in other mutants, cells divide that do not normally do so. The mutants differ in the specificities of their defects, so that it is possible to identify mutations that affect some cell lineages but not others. These mutants define 14 complementation groups, which have been mapped. The abnormal phenotype of most of the cell-lineage mutants results from a single recessive mutation; however, the excessive cell divisions characteristic of one strain, CB1322, require the presence of two unlinked recessive mutations. All 24 cell-lineage mutants display incomplete penetrance and/or variable expressivity. Three of the mutants are suppressed by pleiotropic suppressors believed to be specific for null alleles, suggesting that their phenotypes result from the complete absence of gene activity.


Development ◽  
1992 ◽  
Vol 116 (4) ◽  
pp. 943-952 ◽  
Author(s):  
X. Cui ◽  
C.Q. Doe

Cell diversity in the Drosophila central nervous system (CNS) is primarily generated by the invariant lineage of neural precursors called neuroblasts. We used an enhancer trap screen to identify the ming gene, which is transiently expressed in a subset of neuroblasts at reproducible points in their cell lineage (i.e. in neuroblast ‘sublineages’), suggesting that neuroblast identity can be altered during its cell lineage. ming encodes a predicted zinc finger protein and loss of ming function results in precise alterations in CNS gene expression, defects in axonogenesis and embryonic lethality. We propose that ming controls cell fate within neuroblast cell lineages.


2020 ◽  
Author(s):  
Liana Fasching ◽  
Yeongjun Jang ◽  
Simone Tomasi ◽  
Jeremy Schreiner ◽  
Livia Tomasini ◽  
...  

AbstractPost-zygotic mosaic mutations can be used to track cell lineages in humans. By using cell cloning and induced pluripotent cell lines, we analyzed early cell lineages in two living individuals (a patient and a control), and a postmortem human specimen. Of ten reconstructed post-zygotic divisions, none resulted in balanced contributions of daughter lineages to tissues. In both living individuals one of two lineages from the first cleavage was dominant across tissues, with 90% frequency in blood. We propose that the efficiency of DNA repair contributes to lineage imbalance. Allocation of lineages in postmortem brain correlated with anterior-posterior axis, associating lineage history with cell fate choices in embryos. Recurrence of germline variants as mosaic suggested that certain loci may be particularly susceptible to mutagenesis. We establish a minimally invasive framework for defining cell lineages in any living individual, which paves the way for studying their relevance in health and disease.


Blood ◽  
1986 ◽  
Vol 67 (5) ◽  
pp. 1240-1243
Author(s):  
M Keinanen ◽  
S Knuutila ◽  
CD Bloomfield ◽  
E Elonen ◽  
A de la Chapelle

To determine the hematopoietic cell lineage of mitotic cells in human bone marrow on direct examination and after 24-hour culture, marrow mitoses from four healthy individuals were studied, using a new technique that allows analysis of karyotypes in cells whose cell membrane and cytoplasm have been preserved. Mitoses were identified as being of erythroid lineage by immunofluorescent staining for surface glycophorin A and as being of granulocytic lineage by cytoplasmic staining for Sudan black B. On direct marrow examination without prior culture, the great majority of mitoses (74% to 90%) were of erythroid lineage; only a few (0% to 10%) were granulocytic. After 24-hour culture, the percentage of erythroid mitoses (15% to 40%) decreased, while the percentage of granulocytic mitoses (58% to 87%) increased strikingly. These data indicate that mitotic cells of different hematopoietic cell lineages predominate in marrow at different culture times and offer a plausible explanation for the high frequency of normal karyotypes in acute myeloid leukemia after direct marrow cytogenetic evaluation.


2017 ◽  
Vol 114 (4) ◽  
pp. 758-763 ◽  
Author(s):  
Kyoichi Hashimoto ◽  
Yosuke Yamada ◽  
Katsunori Semi ◽  
Masaki Yagi ◽  
Akito Tanaka ◽  
...  

The spectrum of genetic mutations differs among cancers in different organs, implying a cellular context-dependent effect for genetic aberrations. However, the extent to which the cellular context affects the consequences of oncogenic mutations remains to be fully elucidated. We reprogrammed colon tumor cells in an ApcMin/+ (adenomatous polyposis coli) mouse model, in which the loss of the Apc gene plays a critical role in tumor development and subsequently, established reprogrammed tumor cells (RTCs) that exhibit pluripotent stem cell (PSC)-like signatures of gene expression. We show that the majority of the genes in RTCs that were affected by Apc mutations did not overlap with the genes affected in the intestine. RTCs lacked pluripotency but exhibited an increased expression of Cdx2 and a differentiation propensity that was biased toward the trophectoderm cell lineage. Genetic rescue of the mutated Apc allele conferred pluripotency on RTCs and enabled their differentiation into various cell types in vivo. The redisruption of Apc in RTC-derived differentiated cells resulted in neoplastic growth that was exclusive to the intestine, but the majority of the intestinal lesions remained as pretumoral microadenomas. These results highlight the significant influence of cellular context on gene regulation, cellular plasticity, and cellular behavior in response to the loss of the Apc function. Our results also imply that the transition from microadenomas to macroscopic tumors is reprogrammable, which underscores the importance of epigenetic regulation on tumor promotion.


Development ◽  
1996 ◽  
Vol 122 (3) ◽  
pp. 997-1005 ◽  
Author(s):  
J.C. Larkin ◽  
N. Young ◽  
M. Prigge ◽  
M.D. Marks

Arabidopsis trichomes are single-celled epidermal hairs that serve as a useful model for the study of plant cell differentiation. An examination of the distribution of trichomes early in their development revealed that developing trichomes occur adjacent to another trichome much less frequently than would be expected by chance. Clonal analysis of epidermal cell lineages ruled out a role for cell lineage in generating the observed minimum-distance spacing pattern. Taken together, these results are consistent with a role for lateral inhibition in the control of trichome development. We also report the identification of a new locus, Reduced Trichome Number (RTN), which affects the initiation of trichomes. This locus was initially detected by the reduced number of leaf trichomes on Landsberg erecta plants compared to that on Columbia plants. Quantitative Trait Locus mapping revealed that more than 73% of the variation in trichome number was due to a major locus near erecta on chromosome 2. The reduced number of trichomes conditioned by the Landsberg erecta allele of this locus appeared to be due to an early cessation of trichome initiation. The implications of these observations are discussed with regard to previously published models of trichome development.


Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 1-12 ◽  
Author(s):  
G.M. Technau

The mechanisms leading to the commitment of a cell to a particular fate or to restrictions in its developmental potencies represent a problem of central importance in developmental biology. Both at the genetic and at the molecular level, studies addressing this topic using the fruitfly Drosophila melanogaster have advanced substantially, whereas, at the cellular level, experimental techniques have been most successfully applied to organisms composed of relatively large and accessible cells. The combined application of the different approaches to one system should improve our understanding of the process of commitment as a whole. Recently, a method has been devised to study cell lineage in Drosophila embryos at the single cell level. This method has been used to analyse the lineages, as well as the state of commitment of single cell progenitors from various ectodermal, mesodermal and endodermal anlagen and of the pole cells. The results obtained from a clonal analysis of wild-type larval structures are discussed in this review.


Development ◽  
1992 ◽  
Vol 116 (4) ◽  
pp. 855-863 ◽  
Author(s):  
C.Q. Doe

The first step in generating cellular diversity in the Drosophila central nervous system is the formation of a segmentally reiterated array of neural precursor cells, called neuroblasts. Subsequently, each neuroblast goes through an invariant cell lineage to generate neurons and/or glia. Using molecular lineage markers, I show that (1) each neuroblast forms at a stereotyped time and position; (2) the neuroblast pattern is indistinguishable between thoracic and abdominal segments; (3) the development of individual neuroblasts can be followed throughout early neurogenesis; (4) gene expression in a neuroblast can be reproducibly modulated during its cell lineage; (5) identified ganglion mother cells form at stereotyped times and positions; and (6) the cell lineage of four well-characterized neurons can be traced back to two identified neuroblasts. These results set the stage for investigating neuroblast specification and the mechanisms controlling neuroblast cell lineages.


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