In vitro growth kinetics of mouse trisomies 12 and 19

Nielsén, Karin; Marcus, Menashe; Gropp, A.

doi:10.1111/j.1601-5223.1985.tb00468.x

Cited by 8 publications

(3 citation statements)

References 19 publications

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“…S6) was increased in trisomic cell lines. Cell proliferation was also impaired in primary cells from humans with Down Syndrome (Trisomy 21) but a specific cell cycle defect was not observed either (15,16). It is possible that progression through the cell cycle is slowed overall in trisomic mouse and human cells.…”

Section: Cell Volume Is Increased In Trisomic Cellsmentioning

confidence: 99%

Aneuploidy Affects Proliferation and Spontaneous Immortalization in Mammalian Cells

Williams

Prabhu

Hunter

et al. 2008

Science

565

601

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Aneuploidy, an incorrect chromosome number, is the leading cause of miscarriages and mental retardation in humans and is a hallmark of cancer. We examined the effects of aneuploidy on primary mouse cells by generating a series of cell lines that carry an extra copy of one of four mouse chromosomes. In all four trisomic lines proliferation was impaired and metabolic properties were altered. Immortalization, the acquisition of the ability to proliferate indefinitely, was also affected by the presence of an additional copy of certain chromosomes. Our data indicate that aneuploidy decreases not only organismal but also cellular fitness and elicits traits that are shared between different aneuploid cells.

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Section: Cell Volume Is Increased In Trisomic Cellsmentioning

confidence: 99%

Aneuploidy Affects Proliferation and Spontaneous Immortalization in Mammalian Cells

Williams

Prabhu

Hunter

et al. 2008

Science

565

601

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“…Postzygotic reproductive barriers concern all the events that occur after fertilization, such as reduced hybrid viability and fertility, while prezygotic reproductive barriers concern isolation of sexual partners via ecological, temporal or behavioral isolation. Pheromones play a key role in pre-mating recognition of sexual partners [2]. These compounds are defined as substances released by an animal that are able to induce specific behavioral and/or endocrinological reactions in a sexual partner of the same species [3].…”

Section: Introductionmentioning

confidence: 99%

The evolutionary history of the SAL1 gene family in eutherian mammals

et al. 2011

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BackgroundSAL1 (salivary lipocalin) is a member of the OBP (Odorant Binding Protein) family and is involved in chemical sexual communication in pig. SAL1 and its relatives may be involved in pheromone and olfactory receptor binding and in pre-mating behaviour. The evolutionary history and the selective pressures acting on SAL1 and its orthologous genes have not yet been exhaustively described. The aim of the present work was to study the evolution of these genes, to elucidate the role of selective pressures in their evolution and the consequences for their functions.ResultsHere, we present the evolutionary history of SAL1 gene and its orthologous genes in mammals. We found that (1) SAL1 and its related genes arose in eutherian mammals with lineage-specific duplications in rodents, horse and cow and are lost in human, mouse lemur, bushbaby and orangutan, (2) the evolution of duplicated genes of horse, rat, mouse and guinea pig is driven by concerted evolution with extensive gene conversion events in mouse and guinea pig and by positive selection mainly acting on paralogous genes in horse and guinea pig, (3) positive selection was detected for amino acids involved in pheromone binding and amino acids putatively involved in olfactory receptor binding, (4) positive selection was also found for lineage, indicating a species-specific strategy for amino acid selection.ConclusionsThis work provides new insights into the evolutionary history of SAL1 and its orthologs. On one hand, some genes are subject to concerted evolution and to an increase in dosage, suggesting the need for homogeneity of sequence and function in certain species. On the other hand, positive selection plays a role in the diversification of the functions of the family and in lineage, suggesting adaptive evolution, with possible consequences for speciation and for the reinforcement of prezygotic barriers.

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“…Of course, the prolonged cell cycle, selective disadvantage and fetal growth retardation could merely be nonspecific effects of chromosomal imbalance (Mittwoch 1971). However, while some authors have demonstrated a prolonged rate of cellular proliferation in human fibroblast (Kaback & Bernstein 1970, Schneider & Epstein 1972, Segal & McCoy 1973, Cure et al 1974, Paton et al 1974 and murine (Hongell 1981, Hongell & Gropp 1982 autosomal trisomies, others have found either no significant difference in trisomic human fibroblasts (Kukharenko et al 1974, Hoehn et al 1980, Kajii et al 1980, Hassold & Sandison 1983, trisomic human lymphocytes (Crossen & Morgan 1980, Frias & Carnevale 1983 and murine trisomies (Gropp 1982, Nielsen et al 1985, or even a decrease in cell cycle time of cells with trisomy 21 (Heidemann et al 1983). In addition, seventy of effect on the mitotic cycle has not correlated with amount of additional or missing chromatin (Epstein 1986).…”

Section: Discussionmentioning

confidence: 98%

Growth disadvantage of 45,X and 46,X,del (X) (p11) fibroblasts

Verp

Rosinsky²,

Beau

et al. 1988

Clinical Genetics

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We have previously shown that cell generation time (CGT) is prolonged in 45,X and certain X‐deletion fibroblast lines (Simpson & Le Beau 1981). A consequence of that finding should be that cells with 45,X or an X‐structural abnormality are at a competitive disadvantage when cocultivated with 46,XX cells. To test this hypothesis we prepared 15 mixtures of cells from combinations of 9 different cell lines: four 45,X; one 46,Xdel(X)(p11); and four 46,XX. Each culture was monitored cytogenetically at frequent passage intervals for the percentage of the two cell lines. Significant differences were found between normal and abnormal lines in culture predominance, in the order predicted by our hypothesis (p<0.01). The specific mechanism by which absence of an X chromosome confers growth disadvantage is unknown, but is consistent with prolongation of CGT. Prolongation of CGT could also be responsible for the embryonic lethality, intrauterine growth retardation, short stature, and somatic anomalies commonly observed in individuals with absent or aberrant X chromosomes.

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In vitro growth kinetics of mouse trisomies 12 and 19

Cited by 8 publications

References 19 publications

Aneuploidy Affects Proliferation and Spontaneous Immortalization in Mammalian Cells

Aneuploidy Affects Proliferation and Spontaneous Immortalization in Mammalian Cells

The evolutionary history of the SAL1 gene family in eutherian mammals

Growth disadvantage of 45,X and 46,X,del (X) (p11) fibroblasts

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