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Fragmentation of animal and plant populations typically leads to genetic erosion and increased probability of extirpation. Although these effects can usually be reversed by re-establishing gene flow between population fragments, managers sometimes fail to do so due to fears of outbreeding depression (OD). Rapid development of OD is due primarily to adaptive differentiation from selection or fixation of chromosomal variants. Fixed chromosomal variants can be detected empirically. We used an extended form of the breeders' equation to predict the probability of OD due to adaptive differentiation between recently isolated population fragments as a function of intensity of selection, genetic diversity, effective population sizes, and generations of isolation. Empirical data indicated that populations in similar environments had not developed OD even after thousands of generations of isolation. To predict the probability of OD, we developed a decision tree that was based on the four variables from the breeders' equation, taxonomic status, and gene flow within the last 500 years. The predicted probability of OD in crosses between two populations is elevated when the populations have at least one of the following characteristics: are distinct species, have fixed chromosomal differences, exchanged no genes in the last 500 years, or inhabit different environments. Conversely, the predicted probability of OD in crosses between two populations of the same species is low for populations with the same karyotype, isolated for <500 years, and that occupy similar environments. In the former case, we recommend crossing be avoided or tried on a limited, experimental basis. In the latter case, crossing can be carried out with low probability of OD. We used crosses with known results to test the decision tree and found that it correctly identified cases where OD occurred. Current concerns about OD in recently fragmented populations are almost certainly excessive. La fragmentación de poblaciones animales y vegetales típicamente lleva a la erosión genética y al incremento de la probabilidad de extirpación. Aunque estos efectos generalmente se pueden revertir mediante el restablecimiento del flujo genético entre los fragmentos de poblaciones, los manejadores a veces fallan debido al temor a la depresión exogámica (DEX). El rápido desarrollo de la DEX se debe principalmente a la diferenciación adaptativa de la selección o fijación de variantes cromosómicas. Las variantes cromosómicas fijadas pueden ser detectadas empíricamente. Utilizamos una forma extendida de la ecuación de criadores para predecir la probabilidad de DEX debido a la diferenciación adaptativa entre fragmentos de poblaciones aisladas recientemente como una función de la intensidad de selección, la diversidad genética, el tamaño poblacional efectivo y las generaciones en aislamiento. Los datos empíricos indicaron que poblaciones en ambientes similares no habían desarrollado DEX aun después de mil generaciones en aislamiento. Para predecir la probabilidad de DEX, desarrollamos un árbol dedecisiones basado en las 4 variables de la ecuación de criadores, el estatus taxonómico y el flujo génico durante los últimos 500 años. La probabilidad predicha de DEX es alta en cruzas entre dos poblaciones cuando las poblaciones tienen por lo menos una de las siguientes características: son especies diferentes, tienen diferencias en cromosomas fijados, no intercambiaron genes durante los últimos 500 años o habitan en ambientes diferentes. Por el contrario, la probabilidad predicha de DEX es baja en cruzas entre dos poblacionesde la misma especie cuando las poblaciones tienen el mismo cariotipo, han estado aisladas por <500 años y ocupan ambientes similares. En el primer caso, recomendamos evitar la cruza o probarla en un nivel limitado, experimental. En el segundo caso, la cruza puede llevarse a cabo con baja probabilidad de DEX. Utilizamos cruzas con resultados conocidos para probar el árbol de decisiones y encontramos que este identifico casos correctamente cuando ocurrió DEX. Las preocupaciones actuales sobre DEX en poblaciones fragmentadas recientemente con toda seguridad son excesivas.

Cancer Cytogenetics, 3rd Edition, offers a comprehensive, expanded, and up-to-date review of recent dramatic advances in this area and incorporates a vast amount of new data from the latest basic and clinical investigations. Edited by two leading experts, and now involving a new panel of international experts, the book offers an authoritative description of neoplastic processes at the chromosomal level of genomic organization. Researchers in cytogenetics, medical and molecular genetics, cellular and molecular biology, cancer research, clinical oncology, and hematology will find this reference both thorough and authoritative.

Panama disease of banana, caused by the fungus Fusarium oxysporum f. sp. cubense, is a serious constraint both to the commercial production of banana and cultivation for subsistence agriculture. Previous work has indicated that F. oxysporum f. sp. cubense consists of several clonal lineages that may be genetically distant. In this study we tested whether lineages of the Panama disease pathogen have a monophyletic origin by comparing DNA sequences of nuclear and mitochondrial genes. DNA sequences were obtained for translation elongation factor 1 alpha and the mitochondrial small subunit ribosomal RNA genes for F. oxysporum strains from banana, pathogenic strains from other hosts and putatively nonpathogenic isolates of F. oxysporum. Cladograms for the two genes were highly concordant and a partition-homogeneity test indicated the two datasets could be combined. The tree inferred from the combined dataset resolved five lineages corresponding to \"F. oxysporum f. sp. cubense\" with a large dichotomy between two taxa represented by strains most commonly isolated from bananas with Panama disease. The results also demonstrate that the latter two taxa have significantly different chromosome numbers. F. oxysporum isolates collected as nonpathogenic or pathogenic to other hosts that have very similar or identical elongation factor 1 alpha and mitochondrial small subunit genotypes as banana pathogens were shown to cause little or no disease on banana. Taken together, these results indicate Panama disease of banana is caused by fungi with independent evolutionary origins

Folate deficiency causes massive incorporation of uracil into human DNA (4 million per cell) and chromosome breaks. The likely mechanism is the deficient methylation of dUMP to dTMP and subsequent incorporation of uracil into DNA by DNA polymerase. During repair of uracil in DNA, transient nicks are formed; two opposing nicks could lead to chromosome breaks. Both high DNA uracil levels and elevated micronucleus frequency (a measure of chromosome breaks) are reversed by folate administration. A significant proportion of the U.S. population has low folate levels, in the range associated with elevated uracil misincorporation and chromosome breaks. Such breaks could contribute to the increased risk of cancer and cognitive defects associated with folate deficiency in humans

El comportamiento meiótico es de gran importancia para el desarrollo de programas de mejoramiento genético, especialmente en especies como la vainilla (Vanilla planifolia Jacks.), que se ven severamente afectadas por diversos factores bióticos y abióticos derivados de su estrecha base genética. Por ello, el presente trabajo se planteó con el objetivo de evaluar el comportamiento meiótico del morfotipo comercial \"Mansa\" del municipio de Papantla de Olarte, Veracruz, México. Para ello, se colectaron botones florales de diferentes tamaños y se fijaron en Carnoy, utilizando la técnica de la calabaza, seguido de una tinción con acetocarmín al 2% (p/v) para observar claramente todas las etapas del proceso meiótico.  Se observó un comportamiento meiótico normal y un número de cromosomas haploides (n = 8). Estos resultados pueden ser útiles para el desarrollo de programas de mejora de este cultivo.

Somatic chromosomes of Caesalpinia spinosa (Feuillée ex Molina) Kuntze, “Tara”, wild populations of Huinco and Palca (Junín) regions were studied. The specie were diploid (2n=24). Chromosomes were small. The karyotypes showed the same chromosome number, they found differences in morphological parameters of the same, with the karyotype formula for the town of Huinco: 6m + 6 sm and the town of Palca: 5m + 7 sm.

Milenariamente los agricultores han seleccionado de manera empírica el material de siembra de sus cultivos. Recientemente, de manera sistemática y con base en conocimiento teórico y práctico, los científicos, durante décadas, han venido produciendo variedades, híbridos y clones en todas las especies comerciales comestibles y no comestibles que existen hoy en día. Estos procesos se enmarcan en el mejoramiento genético de plantas (Fitomejoramiento), que a través del tiempo sigue evolucionando, como resultado de la aparición e integración de nuevas tecnologías para lograr procesos más rápidos, más eficientes y menos costosos.

The Mi locus of tomato confers resistance to root knot nematodes. Tomato DNA spanning the locus was isolated as bacterial artificial chromosome clones, and 52 kb of contiguous DNA was sequenced. Three open reading frames were identified with similarity to cloned plant disease resistance genes. Two of them, Mi-1.1 and Mi-1.2, appear to be intact genes; the third is a pseudogene. A 4-kb mRNA hybridizing with these genes is present in tomato roots. Complementation studies using cloned copies of Mi-1.1 and Mi-1.2 indicated that Mi-1.2, but not Mi-1.1, is sufficient to confer resistance to a susceptible tomato line with the progeny of transformants segregating for resistance. The cloned gene most similar to Mi-1.2 is Prf, a tomato gene required for resistance to Pseudomonas syringae. Prf and Mi-1.2 share several structural motifs, including a nucleotide binding site and a leucine-rich repeat region, that are characteristic of a family of plant proteins, including several that are required for resistance against viruses, bacteria, fungi, and now, nematodes

The role of imprinting in body composition was investigated in an experimental cross between Chinese Meishan pigs and commercial Dutch pigs. A whole-genome scan revealed significant evidence for five quantitative trait loci (QTL) affecting body composition, of which four were imprinted. Imprinting was tested with a statistical model that separated the expression of paternally and maternally inherited alleles. For back fat thickness, a paternally expressed QTL was found on Sus scrofa chromosome 2 (SSC2), and a Mendelian-expressed QTL was found on SSC7. In the same region of SSC7, a maternally expressed QTL affecting muscle depth was found. Chromosome 6 harbored a maternally expressed QTL on the short arm and a paternally expressed QTL on the long arm, both affecting intramuscular fat content. The individual QTL explained from 2% up to 10% of the phenotypic variance. The known homologies to human and mouse did not reveal positional candidate genes. This study demonstrates that testing for imprinting should become a standard procedure to unravel the genetic control of multifactorial traits.