scholarly journals Symmetric Inheritance of Histones H3 in Drosophila Male Germline Stem Cell Divisions

2021 ◽  
Author(s):  
Julie Ray ◽  
Keith A. Maggert
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Germ Line ◽  
Germline Stem Cell ◽  
Cell Nuclei ◽  
Cell Divisions ◽  
Regulatory Information ◽  
Alternative Hypotheses ◽  
Stem Cell Divisions ◽  
Gene Regulatory

Mitotically-stable epigenetic memory requires a mechanism for the maintenance of gene-regulatory information through the cell division cycle. Typically DNA-protein contacts are disrupted by DNA replication, but in some cases locus- specific association between DNA and overlying histones may appear to be maintained, providing a plausible mechanism for the transmission of histone-associated gene-regulatory information to daughter cells. Male Drosophila melanogaster testis germ stem cell divisions seem a clear example of such inheritance, as previously chromatin-bound histone H3.2 proteins (presumably with their post-translational modifications intact) have been reported to be retained in the germ stem cell nuclei, while newly synthesized histones are incorporated exclusively into daughter spermatogonial chromosomes. To investigate the rate of errors in this selective partitioning that may lead to defects in the epigenetic identity of germ stem cells, we employed a photoswitchable Dendra2 moiety as a C-terminal fusion on Histones H3; we could thereby discriminate histones translated before photoswitching and those translated after. We found instead that male germ line stem cell divisions show no evidence of asymmetric histone partitioning, even after a single division, and thus no evidence for locus-specific retention of either Histone H3.2 or Histone H3.3. We considered alternative hypotheses for the appearance of asymmetry and find that previous reports of asymmetric histone distribution in male germ stem cells can be satisfactorily explained by asynchrony between subsequent sister stem cell and spermatogonial divisions.

Drosophila Mitochondrial Genetics: Evolution of Heteroplasmy Through Germ Line Cell Divisions

Genetics ◽  
1987 ◽  
Vol 117 (4) ◽  
pp. 687-696 ◽  
Author(s):  
Michel Solignac ◽  
Jean Génermont ◽  
Monique Monnerot ◽  
Jean-Claude Mounolou
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Germ Line ◽  
Female Offspring ◽  
Mitochondrial Genetics ◽  
Germ Line Cell ◽  
Cell Divisions ◽  
Drosophila Mauritiana ◽  
Mitochondrial Genotype ◽  
Stem Cell Division

ABSTRACT The mitochondrial genotype of all F1 female offspring (426 individuals) of a single Drosophila mauritiana female, heteroplasmic for two types of mtDNA (a short and a long genome), was established. All descendants were heteroplasmic. The earliest eggs laid by this female show the cytoplasmic genetic structure of ovariole stem cells at the end of development. Cohorts of females from the eggs laid day after day by this female, throughout the 31 days of its life, provide information on the evolution of the mitochondrial genotypes in the course of successive divisions of stem cells. An increase of the percentage of long DNA in offspring was observed as the female aged. Moreover, the variance of the genotypes increases as rounds of stem cell division progress. These results are supported by observations based on the adults issued from the early and late eggs, for three additional heteroplasmic females.

scholarly journals Variation in cancer risk among tissues can be explained by the number of stem cell divisions

Science ◽  
2015 ◽  
Vol 347 (6217) ◽  
pp. 78-81 ◽  
Author(s):  
Cristian Tomasetti ◽  
Bert Vogelstein
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Dna Replication ◽  
Environmental Factors ◽  
Cancer Risk ◽  
Strongly Correlated ◽  
Cell Divisions ◽  
Human Cancers ◽  
Different Types ◽  
Stem Cell Divisions

Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue’s homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to “bad luck,” that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes.

scholarly journals G-Protein signaling accelerates stem cell divisions in Drosophila males

2018 ◽  
Author(s):  
Manashree Malpe ◽  
Leon F. McSwain ◽  
Karl Kudyba ◽  
Chun L. Ng ◽  
Jennie Nicholson ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
G Protein ◽  
G Proteins ◽  
Adult Stem Cells ◽  
Dominant Negative ◽  
Tissue Loss ◽  
Germline Stem Cell ◽  
Post Injury ◽  
Stem Cell Divisions

AbstractAdult stem cells divide to renew the stem cell pool and replenish specialized cells that are lost due to death or usage. However, little is known about the mechanisms regulating how stem cells adjust to a demand for specialized cells. A failure of the stem cells to respond to this demand can have serious consequences, such as tissue loss, or prolonged recovery post injury.Here, we challenge the male germline stem cells (GSCs) of Drosophila melanogaster for the production of specialized cells using mating experiments. We show that repeated mating reduced the sperm pool and accelerated germline stem cell (GSC) divisions. The increase in GSC divisions depended on the activity of the highly conserved G-proteins. Germline expression of RNA-Interference (RNA-i) constructs against G-proteins or a dominant negative G-protein eliminated the increase in GSC divisions in mated males. Consistent with a role for the G-proteins in the regulation of GSC divisions, RNA-i against seven out of 35 G-protein coupled receptors (GPCRs) within the germline cells also eliminated the capability of males to accelerate their GSC divisions in response to mating. Our data show that GSCs are receptive to GPCR stimulus, potentially through a network of interactions among multiple signaling pathways.

scholarly journals Asymmetric nuclear division of neural stem cells contributes to the formation of sibling nuclei with different identities

2020 ◽  
Author(s):  
Chantal Roubinet ◽  
Ian J. White ◽  
Buzz Baum
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Neural Stem Cells ◽  
Daughter Cell ◽  
Nuclear Division ◽  
Cell Nuclei ◽  
Cell Fates ◽  
Asymmetric Divisions ◽  
Stem Cell Divisions ◽  
Multicellular Organisms

AbstractCellular diversity in multicellular organisms is often generated via asymmetric divisions. In the fly, for example, neural stem cells divide asymmetrically to generate a large self-renewing stem cell and a smaller sibling that differentiates. Efforts to understand how these different cell fates are generated have focused on the asymmetric segregation of cortically-localised transcription factors at division, which preferentially enter single daughter cell nuclei to change their fate. However, we find that the nuclear compartment in these cells remains intact throughout mitosis and is asymmetrically inherited, giving rise to sibling nuclei that differ profoundly in size, envelope composition and fate markers. These data reveal the importance of considering nuclear remodelling during stem cell divisions, and show how daughter cell fates depend on the coordination of the asymmetric inheritance of cortical fate markers with asymmetric nuclear division.

scholarly journals Drosophila small ovary gene ensures germline stem cell maintenance and differentiation by silencing transposons and organising heterochromatin

2018 ◽  
Author(s):  
Ferenc Jankovics ◽  
Melinda Bence ◽  
Rita Sinka ◽  
Anikó Faragó ◽  
László Bodai ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Genetic Interaction ◽  
Position Effect ◽  
Germline Stem Cell ◽  
Physical Interaction ◽  
Position Effect Variegation ◽  
Cell Nuclei ◽  
Transposon Silencing ◽  
Small Ovary

AbstractSelf-renewal and differentiation of stem cells is one of the fundamental biological phenomena relying on proper chromatin organisation. In our study, we describe a novel chromatin regulator encoded by the Drosophila small ovary (sov) gene. We demonstrate that sov is required in both the germline stem cells (GSCs) and the surrounding somatic niche cells to ensure GSC survival and differentiation. Sov maintains niche integrity and function by repressing transposon mobility, not only in the germline, but also in the soma. Protein interactome analysis of Sov revealed a physical interaction between Sov and HP1a. In the germ cell nuclei, Sov co-localises with HP1a, suggesting that Sov affects transposon repression as a component of the heterochromatin. In a position effect variegation assay, we found a dominant genetic interaction between sov and HP1a, indicating their functional cooperation in promoting the spread of heterochromatin. An in vivo tethering assay and FRAP analysis revealed that Sov enhances heterochromatin formation by supporting the recruitment of HP1a to the chromatin. We propose a model in which sov maintains GSC niche integrity by regulating piRNA-mediated transposon silencing as a heterochromatin regulator.Summary statementSmall ovary maintains the integrity of the stem cell niche by regulating piRNA-mediated transposon silencing acting as a key component of the heterochromatin.

The shut-down Gene of Drosophila melanogaster Encodes a Novel FK506-Binding Protein Essential for the Formation of Germline Cysts During Oogenesis

Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 245-256
Author(s):  
Kirsteen Munn ◽  
Ruth Steward
Keyword(s):  
Stem Cells ◽  
Drosophila Melanogaster ◽  
Stem Cell ◽  
Positional Cloning ◽  
Binding Protein ◽  
Protein Domain ◽  
Germline Stem Cell ◽  
Germline Stem Cells ◽  
Fk506 Binding Protein ◽  
Cell Divisions

Abstract In Drosophila melanogaster, the process of oogenesis is initiated with the asymmetric division of a germline stem cell. This division results in the self-renewal of the stem cell and the generation of a daughter cell that undergoes four successive mitotic divisions to produce a germline cyst of 16 cells. Here, we show that shut-down is essential for the normal function of the germline stem cells. Analysis of weak loss-of-function alleles confirms that shut-down is also required at later stages of oogenesis. Clonal analysis indicates that shut-down functions autonomously in the germline. Using a positional cloning approach, we have isolated the shut-down gene. Consistent with its function, the RNA and protein are strongly expressed in the germline stem cells and in 16-cell cysts. The RNA is also present in the germ cells throughout embryogenesis. shut-down encodes a novel Drosophila protein similar to the heat-shock protein-binding immunophilins. Like immunophilins, Shut-down contains an FK506-binding protein domain and a tetratricopeptide repeat. In plants, high-molecular-weight immunophilins have been shown to regulate cell divisions in the root meristem in response to extracellular signals. Our results suggest that shut-down may regulate germ cell divisions in the germarium.

scholarly journals A hybrid model connecting regulatory interactions with stem cell divisions in the root

2021 ◽  
Vol 2 ◽  
Author(s):  
Lisa Van den Broeck ◽  
Ryan J. Spurney ◽  
Adam P. Fisher ◽  
Michael Schwartz ◽  
Natalie M. Clark ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hybrid Model ◽  
Regulatory Networks ◽  
Quiescent Center ◽  
Specific Expression ◽  
Agent Based ◽  
Cell Divisions ◽  
Cell Type Specific Expression ◽  
Stem Cell Divisions ◽  
Cell Niche

Abstract Stem cells give rise to the entirety of cells within an organ. Maintaining stem cell identity and coordinately regulating stem cell divisions is crucial for proper development. In plants, mobile proteins, such as WUSCHEL-RELATED HOMEOBOX 5 (WOX5) and SHORTROOT (SHR), regulate divisions in the root stem cell niche. However, how these proteins coordinately function to establish systemic behaviour is not well understood. We propose a non-cell autonomous role for WOX5 in the cortex endodermis initial (CEI) and identify a regulator, ANGUSTIFOLIA (AN3)/GRF-INTERACTING FACTOR 1, that coordinates CEI divisions. Here, we show with a multi-scale hybrid model integrating ordinary differential equations (ODEs) and agent-based modeling that quiescent center (QC) and CEI divisions have different dynamics. Specifically, by combining continuous models to describe regulatory networks and agent-based rules, we model systemic behaviour, which led us to predict cell-type-specific expression dynamics of SHR, SCARECROW, WOX5, AN3 and CYCLIND6;1, and experimentally validate CEI cell divisions. Conclusively, our results show an interdependency between CEI and QC divisions.

The role of lin-22, a hairy/enhancer of split homolog, in patterning the peripheral nervous system of C. elegans

Development ◽  
1997 ◽  
Vol 124 (15) ◽  
pp. 2875-2888 ◽  
Author(s):  
L.A. Wrischnik ◽  
C.J. Kenyon
Keyword(s):  
Stem Cell ◽  
Regulatory Gene ◽  
Epidermal Cells ◽  
Body Axis ◽  
Wild Type ◽  
Hox Gene ◽  
C Elegans ◽  
Cell Divisions ◽  
Body Regions ◽  
Stem Cell Divisions

In C. elegans, six lateral epidermal stem cells, the seam cells V1-V6, are located in a row along the anterior-posterior (A/P) body axis. Anterior seam cells (V1-V4) undergo a fairly simple sequence of stem cell divisions and generate only epidermal cells. Posterior seam cells (V5 and V6) undergo a more complicated sequence of cell divisions that include additional rounds of stem cell proliferation and the production of neural as well as epidermal cells. In the wild type, activity of the gene lin-22 allows V1-V4 to generate their normal epidermal lineages rather than V5-like lineages. lin-22 activity is also required to prevent additional neurons from being produced by one branch of the V5 lineage. We find that the lin-22 gene exhibits homology to the Drosophila gene hairy, and that lin-22 activity represses neural development within the V5 lineage by blocking expression of the posterior-specific Hox gene mab-5 in specific cells. In addition, in order to prevent anterior V cells from generating V5-like lineages, wild-type lin-22 gene activity must inhibit (directly or indirectly) at least five downstream regulatory gene activities. In anterior body regions, lin-22(+) inhibits expression of the Hox gene mab-5. It also inhibits the activity of the achaete-scute homolog lin-32 and an unidentified gene that we postulate regulates stem cell division. Each of these three genes is required for the expression of a different piece of the ectopic V5-like lineages generated in lin-22 mutants. In addition, lin-22 activity prevents two other Hox genes, lin-39 and egl-5, from acquiring new activities within their normal domains of function along the A/P body axis. Some, but not all, of the patterning activities of lin-22 in C. elegans resemble those of hairy in Drosophila.

scholarly journals Klp10A, a stem cell centrosome-enriched kinesin, balances asymmetries in Drosophila male germline stem cell division

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Cuie Chen ◽  
Mayu Inaba ◽  
Zsolt G Venkei ◽  
Yukiko M Yamashita
Keyword(s):  
Stem Cell ◽  
Cell Division ◽  
Cell Fate ◽  
Germline Stem Cell ◽  
Germline Stem Cells ◽  
Male Germline ◽  
Mother And Daughter ◽  
Stem Cell Divisions ◽  
Stem Cell Division ◽  
Male Germline Stem Cells

Asymmetric stem cell division is often accompanied by stereotypical inheritance of the mother and daughter centrosomes. However, it remains unknown whether and how stem cell centrosomes are uniquely regulated and how this regulation may contribute to stem cell fate. Here we identify Klp10A, a microtubule-depolymerizing kinesin of the kinesin-13 family, as the first protein enriched in the stem cell centrosome in Drosophila male germline stem cells (GSCs). Depletion of klp10A results in abnormal elongation of the mother centrosomes in GSCs, suggesting the existence of a stem cell-specific centrosome regulation program. Concomitant with mother centrosome elongation, GSCs form asymmetric spindle, wherein the elongated mother centrosome organizes considerably larger half spindle than the other. This leads to asymmetric cell size, yielding a smaller differentiating daughter cell. We propose that klp10A functions to counteract undesirable asymmetries that may result as a by-product of achieving asymmetries essential for successful stem cell divisions.

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