scholarly journals The Consequences of Budding versus Binary Fission on Adaptation and Aging in Primitive Multicellularity

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 661
Author(s):  
Hanna Isaksson ◽  
Peter L. Conlin ◽  
Ben Kerr ◽  
William C. Ratcliff ◽  
Eric Libby

Early multicellular organisms must gain adaptations to outcompete their unicellular ancestors, as well as other multicellular lineages. The tempo and mode of multicellular adaptation is influenced by many factors including the traits of individual cells. We consider how a fundamental aspect of cells, whether they reproduce via binary fission or budding, can affect the rate of adaptation in primitive multicellularity. We use mathematical models to study the spread of beneficial, growth rate mutations in unicellular populations and populations of multicellular filaments reproducing via binary fission or budding. Comparing populations once they reach carrying capacity, we find that the spread of mutations in multicellular budding populations is qualitatively distinct from the other populations and in general slower. Since budding and binary fission distribute age-accumulated damage differently, we consider the effects of cellular senescence. When growth rate decreases with cell age, we find that beneficial mutations can spread significantly faster in a multicellular budding population than its corresponding unicellular population or a population reproducing via binary fission. Our results demonstrate that basic aspects of the cell cycle can give rise to different rates of adaptation in multicellular organisms.

2015 ◽  
Vol 3 (2) ◽  
Author(s):  
Naresh Singla ◽  
Mamandeep Kaur

The growth of agriculture and allied sectors is critical for the Indian economy as about 49 percent of the population is directly or indirectly dependent on agriculture. During the last decade and so, the agriculture sector has undergone profound changes resulting in sharp deceleration in its growth. The study has attempted to analyze growth and performance of the agriculture sector in India since 1980-81 and tries to comprehend some of the factors responsible for the deceleration in growth. The study has shown that agriculture sector has been able to show tremendous improvement in expansion of area and production of food grain and non-food grain crops. However, there are so many underlying factors responsible for slowdown of the agricultural growth. Some of the factors identified include: Increase in area under non-agriculture uses, excessive dependence on rain fed farming, increase in number of agricultural labourers, reducing size of the operation holdings, over use of agri-inputs, inequity in the distribution of agriculture credit along with sharp deceleration in public gross capital formation in agriculture etc. The study pointed in order to achieve higher growth rate, there is a need to enhance the gross capital formation in agriculture sector particularly on irrigation so that more area can be brought under assured irrigation. Bringing equity in distribution of agricultural credit coupled with judicious and need-based agricultural inputs are some of the other recommendations drawn based upon the study.


1988 ◽  
Vol 53 (12) ◽  
pp. 2995-3013
Author(s):  
Emerich Erdös ◽  
Jindřich Leitner ◽  
Petr Voňka ◽  
Josef Stejskal ◽  
Přemysl Klíma

For a quantitative description of the epitaxial growth rate of gallium arsenide, two models are proposed including two rate controlling steps, namely the diffusion of components in the gas phase and the surface reaction. In the models considered, the surface reaction involves a reaction triple - or quadruple centre. In both models three mechanisms are considered which differ one from the other by different adsorption - and impact interaction of reacting particles. In every of the six cases, the pertinent rate equations were derived, and the models have been confronted with the experimentally found dependences of the growth rate on partial pressures of components in the feed. The results are discussed with regard to the plausibility of individual mechanisms and of both models, and also with respect to their applicability and the direction of further investigations.


Author(s):  
Samuel K. Cohn, Jr.

This book challenges a dominant hypothesis in the study of epidemics. From an interdisciplinary array of scholars, a consensus has emerged: invariably, epidemics in past times provoked class hatred, blame of the ‘other’, or victimization of the diseases’ victims. It is also claimed that when diseases were mysterious, without cures or preventive measures, they more readily provoked ‘sinister connotations’. The evidence for these assumptions, however, comes from a handful of examples—the Black Death, the Great Pox at the end of the sixteenth century, cholera riots of the 1830s, and AIDS, centred almost exclusively on the US experience. By investigating thousands of descriptions of epidemics, reaching back before the fifth-century BCE Plague of Athens to the eruption of Ebola in 2014, this study traces epidemics’ socio-psychological consequences across time and discovers a radically different picture. First, scholars, especially post-AIDS, have missed a fundamental aspect of the history of epidemics: their remarkable power to unify societies across class, race, ethnicity, and religion, spurring self-sacrifice and compassion. Second, hatred and violence cannot be relegated to a time when diseases were mysterious, before the ‘laboratory revolution’ of the late nineteenth century: in fact, modernity was the great incubator of a disease–hate nexus. Third, even with diseases that have tended to provoke hatred, such as smallpox, poliomyelitis, plague, and cholera, blaming ‘the other’ or victimizing disease bearers has been rare. Instead, the history of epidemics and their socio-psychological consequences has been richer and more varied than scholars and public intellectuals have heretofore allowed.


Chromosoma ◽  
2021 ◽  
Vol 130 (1) ◽  
pp. 15-25
Author(s):  
Phuong T. N. Hoang ◽  
Jean-Marie Rouillard ◽  
Jiří Macas ◽  
Ivona Kubalová ◽  
Veit Schubert ◽  
...  

AbstractDuckweeds represent a small, free-floating aquatic family (Lemnaceae) of the monocot order Alismatales with the fastest growth rate among flowering plants. They comprise five genera (Spirodela, Landoltia, Lemna, Wolffiella, and Wolffia) varying in genome size and chromosome number. Spirodela polyrhiza had the first sequenced duckweed genome. Cytogenetic maps are available for both species of the genus Spirodela (S. polyrhiza and S. intermedia). However, elucidation of chromosome homeology and evolutionary chromosome rearrangements by cross-FISH using Spirodela BAC probes to species of other duckweed genera has not been successful so far. We investigated the potential of chromosome-specific oligo-FISH probes to address these topics. We designed oligo-FISH probes specific for one S. intermedia and one S. polyrhiza chromosome (Fig. 1a). Our results show that these oligo-probes cross-hybridize with the homeologous regions of the other congeneric species, but are not suitable to uncover chromosomal homeology across duckweeds genera. This is most likely due to too low sequence similarity between the investigated genera and/or too low probe density on the target genomes. Finally, we suggest genus-specific design of oligo-probes to elucidate chromosome evolution across duckweed genera.


Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 67-77 ◽  
Author(s):  
A Parket ◽  
O Inbar ◽  
M Kupiec

Abstract The Ty retrotransposons are the main family of dispersed repeated sequences in the yeast Saccharomyces cerevisiae. These elements are flanked by a pair of long terminal direct repeats (LTRs). Previous experiments have shown that Ty elements recombine at low frequencies, despite the fact that they are present in 30 copies per genome. This frequency is not highly increased by treatments that cause DNA damage, such as UV irradiation. In this study, we show that it is possible to increase the recombination level of a genetically marked Ty by creating a double-strand break in it. This break is repaired by two competing mechanisms: one of them leaves a single LTR in place of the Ty, and the other is a gene conversion event in which the marked Ty is replaced by an ectopically located one. In a strain in which the marked Ty has only one LTR, the double-strand break is repaired by conversion. We have also measured the efficiency of repair and monitored the progression of the cells through the cell-cycle. We found that in the presence of a double-strand break in the marked Ty, a proportion of the cells is unable to resume growth.


Cells ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 8 ◽  
Author(s):  
Umamaheswari Natarajan ◽  
Thiagarajan Venkatesan ◽  
Vijayaraghavan Radhakrishnan ◽  
Shila Samuel ◽  
Appu Rathinavelu

Gene expression is often altered by epigenetic modifications that can significantly influence the growth ability and progression of cancers. SAHA (Suberoylanilide hydroxamic acid, also known as Vorinostat), a well-known Histone deacetylase (HDAC) inhibitor, can stop cancer growth and metastatic processes through epigenetic alterations. On the other hand, Letrozole is an aromatase inhibitor that can elicit strong anti-cancer effects on breast cancer through direct and indirect mechanisms. A newly developed inhibitor, RG7388 specific for an oncogene-derived protein called MDM2, is in clinical trials for the treatment of various cancers. In this paper, we performed assays to measure the effects of cell cycle arrest resulting from individual drug treatments or combination treatments with SAHA + letrozole and SAHA + RG7388, using the MCF-7 breast cancer cells. When SAHA was used individually, or in combination treatments with RG7388, a significant increase in the cytotoxic effect was obtained. Induction of cell cycle arrest by SAHA in cancer cells was evidenced by elevated p21 protein levels. In addition, SAHA treatment in MCF-7 cells showed significant up-regulation in phospho-RIP3 and MLKL levels. Our results confirmed that cell death caused by SAHA treatment was primarily through the induction of necroptosis. On the other hand, the RG7388 treatment was able to induce apoptosis by elevating BAX levels. It appears that, during combination treatments, with SAHA and RG7388, two parallel pathways might be induced simultaneously, that could lead to increased cancer cell death. SAHA appears to induce cell necroptosis in a p21-dependent manner, and RG7388 seems to induce apoptosis in a p21-independent manner, outlining differential mechanisms of cell death induction. However, further studies are needed to fully understand the intracellular mechanisms that are triggered by these two anti-cancer agents.


2005 ◽  
Vol 25 (23) ◽  
pp. 10315-10328 ◽  
Author(s):  
Yukinori Minoshima ◽  
Tetsuya Hori ◽  
Masahiro Okada ◽  
Hiroshi Kimura ◽  
Tokuko Haraguchi ◽  
...  

ABSTRACT We identified CENP-50 as a novel kinetochore component. We found that CENP-50 is a constitutive component of the centromere that colocalizes with CENP-A and CENP-H throughout the cell cycle in vertebrate cells. To determine the precise role of CENP-50, we examined its role in centromere function by generating a loss-of-function mutant in the chicken DT40 cell line. The CENP-50 knockout was not lethal; however, the growth rate of cells with this mutation was slower than that of wild-type cells. We observed that the time for CENP-50-deficient cells to complete mitosis was longer than that for wild-type cells. Centromeric localization of CENP-50 was abolished in both CENP-H- and CENP-I-deficient cells. Coimmunoprecipitation experiments revealed that CENP-50 interacted with the CENP-H/CENP-I complex in chicken DT40 cells. We also observed severe mitotic defects in CENP-50-deficient cells with apparent premature sister chromatid separation when the mitotic checkpoint was activated, indicating that CENP-50 is required for recovery from spindle damage.


Author(s):  
Sofia Ferreira-Gonzalez ◽  
Daniel Rodrigo-Torres ◽  
Victoria L. Gadd ◽  
Stuart J. Forbes

AbstractCellular senescence is an irreversible cell cycle arrest implemented by the cell as a result of stressful insults. Characterized by phenotypic alterations, including secretome changes and genomic instability, senescence is capable of exerting both detrimental and beneficial processes. Accumulating evidence has shown that cellular senescence plays a relevant role in the occurrence and development of liver disease, as a mechanism to contain damage and promote regeneration, but also characterizing the onset and correlating with the extent of damage. The evidence of senescent mechanisms acting on the cell populations of the liver will be described including the role of markers to detect cellular senescence. Overall, this review intends to summarize the role of senescence in liver homeostasis, injury, disease, and regeneration.


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