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Results for “polyploidy”

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PubMed1979

Polyploidy and domestication: the origin and survival of polyploids in cytotype mixtures.

The origin and survival of a polyploid in a mixture of this polyploid and its parent(s) is reviewed. With several examples a picture is drawn of the interference of cytotypes in a mixture of cytotypes. Some natural polyploids, both wild and domesticated, are very successful. They, like bread wheat and banana, largely replaced their parents. The same is true for some artificial polyploids like autotriploid hybride sugar beet in Europe and autotetraploid perennial ryegrass. But when grown together with their parents for several generations they will disappear from this misture. Although in South America under primitive conditions, diploid, triploid, and tetraploid potatoes are grown, elsewhere only the tetraploids have survived. Various causes are presented to explain why the diploids and triploids succumbed. Autotetraploids of maize, rye, barley, and rice cannot maintain themselves in diploid/tetraploid mixtures. The maintenance of diploid or tetraploid rye varieties is less difficult as both are "self-cleaning" with respect to the other. Only two haploid cultivars exist but they can only maintain themselves with the help of man. It is concluded that the survival chances of a polyploid after its origination is low. Firstly, under conditions of random sampling a rare type has a very small chance of occurring in the next generation. Furthermore, seedset of triploids and tetraploids is often low which limits their survival. In addition, in mixtures of cross-fertilizing diploid and autotetraploids the n gamete has an advantage over the 2n gamete. This limits the survival of the autotetraploids again. It is concluded that our knowledge of the the mutual interference of cytotypes in a cytotype mixture is quite limited. Much more research is needed and some proposals concerning this research are made.

Agriculture↗
PubMed1977

Facultative polyploidy in endocrine tissues.

Adrenal tissue from 44 autopsies and 30 biopsies of thyroid gland were analyzed by flow--and scanning-cytophotometry. Most nuclei were diploid and the 4C fraction ranged from 1.9 to 6.1% according to the technique, but with no significant difference between controls and adenomas, hyperplasias, adenomatous goiters, or two carcinomas of the thyroid gland. The only significant increase of 4C fraction was found in normal adrenals of patients above 50 years of age (P less than 0,025). Similarly constant was the proportion of 8C nuclei which ranged from 0.5 to 1.3 per thousand. However, in one of 23 adenomatous goiters a total polyploidization was was observed. Comparable results in the literature show that the thyroid gland like the epithelium of seminal vesicles can facultatively become polyploidized, in contrast to the obligatory polyploid orgnas namely the liver and heart. This is not related to malignancy.

Adenocarcinoma↗
PubMed2025

Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.

Polyploid Giant Cancer Cells (PGCCs) occur across multiple cancer types and are associated with therapy resistance, genome instability, disease progression, and metastasis. PGCCs can grow through endocycles, a variant cell cycle of alternating Growth (G) and DNA Synthesis (S) phases without cell division. Unlike programmed endocycles that occur during normal tissue development, PGCCs switch from mitotic cycles to unscheduled endocycles in response to stress. PGCCs can subsequently return to error-prone divisions which generate aneuploid daughter cells that contribute to disease progression. However, the regulation of PGCC cell cycles and contributions to cancer are still being defined. Filling this knowledge gap will lead to the development of improved cancer therapies. In this study, we used a molecular-genetic system in the model organism Drosophila melanogaster to examine how oncogenes interact with unscheduled endocycles in vivo. We found that several oncogenes promote bypass of an endocycle arrest, resulting in increased polyploid cell size and DNA content. The extent of this increased growth was dependent on the type of oncogenic mutation. When these polyploid cells returned to division, RasG12V promoted continued divisions of polyploid daughter cells with elevated genome instability. RasG12V expression during transient endocycles and subsequent divisions also induced expression of a matrix metalloprotease and a Wnt pathway ligand. Importantly, RasG12V with transient endocycles enhanced the growth of large, neoplastic tumors. These findings indicate that oncogenic mutations can synergize with transient, unscheduled endocycles to promote tumorigenesis with important broader implications for cancer prognosis and therapies.

Animals↗
PubMed2015

Clonality and intracellular polyploidy in virus evolution and pathogenesis.

In the present article we examine clonality in virus evolution. Most viruses retain an active recombination machinery as a potential means to initiate new levels of genetic exploration that go beyond those attainable solely by point mutations. However, despite abundant recombination that may be linked to molecular events essential for genome replication, herein we provide evidence that generation of recombinants with altered biological properties is not essential for the completion of the replication cycles of viruses, and that viral lineages (near-clades) can be defined. We distinguish mechanistically active but inconsequential recombination from evolutionarily relevant recombination, illustrated by episodes in the field and during experimental evolution. In the field, recombination has been at the origin of new viral pathogens, and has conferred fitness advantages to some viruses once the parental viruses have attained a sufficient degree of diversification by point mutations. In the laboratory, recombination mediated a salient genome segmentation of foot-and-mouth disease virus, an important animal pathogen whose genome in nature has always been characterized as unsegmented. We propose a model of continuous mutation and recombination, with punctuated, biologically relevant recombination events for the survival of viruses, both as disease agents and as promoters of cellular evolution. Thus, clonality is the standard evolutionary mode for viruses because recombination is largely inconsequential, since the decisive events for virus replication and survival are not dependent on the exchange of genetic material and formation of recombinant (mosaic) genomes.

Animals↗