222 research outputs found
Meiotic crossover reduction by virus-induced gene silencing enables the efficient generation of chromosome substitution lines and reverse breeding in Arabidopsis thaliana.
Plant breeding applications exploiting meiotic mutant phenotypes (like the increase or decrease of crossover (CO) recombination) have been proposed over the last years. As recessive meiotic mutations in breeding lines may affect fertility or have other pleiotropic effects, transient silencing techniques may be preferred. Reverse breeding is a breeding technique that would benefit from the transient downregulation of CO formation. The technique is essentially the opposite of plant hybridization: a method to extract parental lines from a hybrid. The method can also be used to efficiently generate chromosome substitution lines (CSLs). For successful reverse breeding, the two homologous chromosome sets of a heterozygous plant must be divided over two haploid complements, which can be achieved by the suppression of meiotic CO recombination and the subsequent production of doubled haploid plants. Here we show the feasibility of transiently reducing CO formation using virus-induced gene silencing (VIGS) by targeting the meiotic gene MSH5 in a wild-type heterozygote of Arabidopsis thaliana. The application of VIGS (rather than using lengthy stable transformation) generates transgene-free offspring with the desired genetic composition: we obtained parental lines from a wild-type heterozygous F1 in two generations. In addition, we obtained 20 (of the 32 possible) CSLs in one experiment. Our results demonstrate that meiosis can be modulated at will in A. thaliana to generate CSLs and parental lines rapidly for hybrid breeding. Furthermore, we illustrate how the modification of meiosis using VIGS can open routes to develop efficient plant breeding strategies
Does livestock predation reflect in negative local perceptions of Ethiopian wolves in South Wollo?
Conservation Biolog
Effectiveness of a LED flashlight technique in reducing livestock depredation by lions (Panthera leo) around Nairobi National Park, Kenya
Conservation Biolog
Boundary relations and generalized resolvents of symmetric operators
The Kre\u{\i}n-Naimark formula provides a parametrization of all selfadjoint
exit space extensions of a, not necessarily densely defined, symmetric
operator, in terms of maximal dissipative (in \dC_+) holomorphic linear
relations on the parameter space (the so-called Nevanlinna families). The new
notion of a boundary relation makes it possible to interpret these parameter
families as Weyl families of boundary relations and to establish a simple
coupling method to construct the generalized resolvents from the given
parameter family. The general version of the coupling method is introduced and
the role of boundary relations and their Weyl families for the
Kre\u{\i}n-Naimark formula is investigated and explained.Comment: 47 page
Prevalence of variations in melanoma susceptibility genes among Slovenian melanoma families
<p>Abstract</p> <p>Background</p> <p>Two high-risk genes have been implicated in the development of CM (cutaneous melanoma). Germline mutations of the CDKN2A gene are found in < 25% of melanoma-prone families and there are only seven families with mutation of the <it>CDK4 </it>gene reported to date. Beside those high penetrance genes, certain allelic variants of the <it>MC1R </it>gene modify the risk of developing the disease.</p> <p>The aims of our study were: to determine the prevalence of germline <it>CDKN2A </it>mutations and variants in members of families with familial CM and in patients with multiple primary CM; to search for possible <it>CDK4 </it>mutations, and to determine the frequency of variations in the <it>MC1R </it>gene.</p> <p>Methods</p> <p>From January 2001 until January 2007, 64 individuals were included in the study. The group included 28 patients and 7 healthy relatives belonging to 25 families, 26 patients with multiple primary tumors and 3 children with CM. Additionally 54 healthy individuals were included as a control group. Mutations and variants of the melanoma susceptibility genes were identified by direct sequencing.</p> <p>Results</p> <p>Seven families with CDKN2A mutations were discovered (7/25 or 28.0%). The L94Q mutation found in one family had not been previously reported in other populations. The D84N variant, with possible biological impact, was discovered in the case of patient without family history but with multiple primary CM. Only one mutation carrier was found in the control group. Further analysis revealed that c.540C>T heterozygous carriers were more common in the group of CM patients and their healthy relatives (11/64 vs. 2/54). One p14ARF variant was discovered in the control group and no mutations of the <it>CDK4 </it>gene were found.</p> <p>Most frequently found variants of the <it>MC1R </it>gene were T314T, V60L, V92M, R151C, R160W and R163Q with frequencies slightly higher in the group of patients and their relatives than in the group of controls, but the difference was statistically insignificant.</p> <p>Conclusion</p> <p>The present study has shown high prevalence of p16INK4A mutations in Slovenian population of familial melanoma patients (37%) and an absence of p14ARF or <it>CDK4 </it>mutations.</p
Coordination activities of human planners during rescheduling: case analysis and event handling procedure
The CHEK2 1100delC mutation identifies families with a hereditary breast and colorectal cancer phenotype
Because of genetic heterogeneity, the identification of breast
cancer-susceptibility genes has proven to be exceedingly difficult. Here,
we define a new subset of families with breast cancer characterized by the
presence of colorectal cancer cases. The 1100delC variant of the cell
cycle checkpoint kinase CHEK2 gene was present in 18% of 55 families with
hereditary breast and colorectal cancer (HBCC) as compared with 4% of 380
families with non-HBCC (P<.001), thus providing genetic evidence for the
HBCC phenotype. The CHEK2 1100delC mutation was, however, not the major
predisposing factor for the HBCC phenotype but appeared to act in synergy
with another, as-yet-unknown susceptibility gene(s). The unequivocal
definition of the HBCC phenotype opens new avenues to search for thi
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