scholarly journals Genetic Changes Accompanying the Evolution of Host Specialization in Drosophila sechellia

Genetics ◽  
2008 ◽  
Vol 181 (2) ◽  
pp. 721-736 ◽  
Author(s):  
Ian Dworkin ◽  
Corbin D. Jones
2021 ◽  
Vol 55 (1) ◽  
Author(s):  
Thomas O. Auer ◽  
Michael P. Shahandeh ◽  
Richard Benton

Defining the mechanisms by which animals adapt to their ecological niche is an important problem bridging evolution, genetics, and neurobiology. We review the establishment of a powerful genetic model for comparative behavioral analysis and neuroecology, Drosophila sechellia. This island-endemic fly species is closely related to several cosmopolitan generalists, including Drosophila melanogaster, but has evolved extreme specialism, feeding and reproducing exclusively on the noni fruit of the tropical shrub Morinda citrifolia. We first describe the development and use of genetic approaches to facilitate genotype/phenotype associations in these drosophilids. Next, we survey the behavioral, physiological, and morphological adaptations of D. sechellia throughout its life cycle and outline our current understanding of the genetic and cellular basis of these traits. Finally, we discuss the principles this knowledge begins to establish in the context of host specialization, speciation, and the neurobiology of behavioral evolution and consider open questions and challenges in the field. Expected final online publication date for the Annual Review of Genetics, Volume 55 is November 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.


2002 ◽  
Vol 92 (3) ◽  
pp. 300-307 ◽  
Author(s):  
Yigal Cohen

In this survey, 799 isolates of Phytophthora infestans collected from potato crops in Israel during 1983 to 2000 were analyzed for mating type and sensitivity to metalaxyl, and 324 were analyzed for race structure. The A2 mating type, first recorded in 1983, fully dominated the pathogen population from 1983 until 1991 (9 years). It was thereafter replaced by the A1 mating type, which dominated the population during 1993 to 2000. Metalaxyl-resistant isolates were first recorded in 1982. During 1983 to 1991, the majority of the isolates were resistant. Isolates with intermediate sensitivity (I) to this fungicide were first observed in 1993, when both A1 and A2 mating types occurred in the population. The proportion of I isolates gradually increased, reaching 39 to 41% in 1997 to 1998, and then declined to ≈15% in 1999 to 2000. Pathogenicity to nine potato differential cultivars was determined for 80 potato isolates collected in 1983 to 1991, to 11 potato differentials in 173 isolates collected in 1993 to 1998, and in 71 potato isolates collected in 1999 to 2000. The first population was composed of 5 races with race 1,3,4,7,8,10 predominating (76%), the second population was composed of 19 races with race 1,3,4,7,8,10,11 predominating (63%), and the third population exhibited 42 (34 new) races with no single predominating race. RG-57 DNA fingerprinting and allozymes loci assays of 23 isolates revealed that isolates collected during 1984 to 1986 belonged to the PO-57 lineage, whereas those collected during 1997 to 1999 belonged to the RFO-39 lineage. Among isolates collected during 1993 to 1995, two unreported DNA fingerprinting patterns were found. Severe late blight epidemics occurred in tomato crops during 1998 to 2000. Of 35 tomato isolates, 28 were A1 and only 7 were A2. Of these tomato isolates, 94% were sensitive to metalaxyl. Almost every isolate had a different race structure on the 11 potato differentials. When inoculated onto three tomato differential cultivars, tomato isolates showed a virulence much more enhanced than potato isolates. The data suggest the Israeli population of P. infestans has passed through three major genetic changes during the past 18 years: in 1983, 1993, and 1999. The recent change included host specialization to tomato.


2013 ◽  
Vol 368 (1632) ◽  
pp. 20130028 ◽  
Author(s):  
David L. Stern ◽  
Nicolás Frankel

In this paper, we provide a historical account of the contribution of a single line of research to our current understanding of the structure of cis -regulatory regions and the genetic basis for morphological evolution. We revisit the experiments that shed light on the evolution of larval cuticular patterns within the genus Drosophila and the evolution and structure of the shavenbaby gene. We describe the experiments that led to the discovery that multiple genetic changes in the cis -regulatory region of shavenbaby caused the loss of dorsal cuticular hairs (quaternary trichomes) in first instar larvae of Drosophila sechellia . We also discuss the experiments that showed that the convergent loss of quaternary trichomes in D. sechellia and Drosophila ezoana was generated by parallel genetic changes in orthologous enhancers of shavenbaby . We discuss the observation that multiple shavenbaby enhancers drive overlapping patterns of expression in the embryo and that these apparently redundant enhancers ensure robust shavenbaby expression and trichome morphogenesis under stressful conditions. All together, these data, collected over 13 years, provide a fundamental case study in the fields of gene regulation and morphological evolution, and highlight the importance of prolonged, detailed studies of single genes.


2014 ◽  
Vol 68 (1) ◽  
pp. 8-15
Author(s):  
Lena Kakasheva-Mazhenkovska ◽  
Vesna Janevska ◽  
Gordana Petrushevska ◽  
Liljana Spasevska ◽  
Neli Basheska

Abstract The stroma of the neoplasm is a highly complex structure built by: specialized mesenchymal cells typical for each tissue surroundings, cancer associated fibroblast/myofibroblast, congenital or acquired immune cells, vascular network with endothelial cells and pericytes, mastocytes, macrophages, leukocytes and adipocytes, all together incorporated in the extracellular matrix. Each neoplasm produces its own unique microenvironment where the tumor grows and modifies. Although most of the cells of the host in the stroma have compulsory tumor suppressor ability, the stroma is changing during the malignant process and it even promotes growth, invasion and metastasis. Genetic changes that occur during the development of the cancer, which are guided by the malignant cells lead to changes in the stroma of the host that will overtake it and adjust it to their own needs. In the early stages of the tumor development and invasion, the basal membrane is degraded and the stroma becomes active and contains an increased number of fibroblasts, inflammatory infiltrate and newly composed capillaries which come into direct contact with the tumor cells. These changes lead to cancer invasion.


Author(s):  
В.А. Бывальцев ◽  
И.А. Степанов ◽  
Е.Г. Белых ◽  
А.И. Яруллина

Цель обзора - анализ современных данных литературы о нарушении внутриклеточных сигнальных путей, играющих ведущую роль в развитии менингиом, генетических и молекулярных профилях данной группы опухолей. К настоящему времени изучено множество аберрантных сигнальных внутриклеточных путей, которые играют важнейшую роль в развитии менингиом головного мозга. Четкое понимание поврежденных внутриклеточных каскадов поможет изучить влияние генетических мутаций и их эффектов на менингиомогенез. Подробное исследование генетического и молекулярного профиля менингиом позволит сделать первый уверенный шаг в разработке более эффективных методов лечения данной группы интракраниальных опухолей. Хромосомы 1, 10, 14, 22 и связанные с ними генные мутации ответственны за рост и прогрессию менингиом. Предполагается, что только через понимание данных генетических повреждений будут реализованы новейшие эффективные методы лечения. Будущая терапия будет включать в себя комбинации таргетных молекулярных агентов, в том числе генную терапию, малые интерферирующие РНК, протонную терапию и другие методы воздействия, как результат дальнейшего изучения генетических и биологических изменений, характерных для менингеальных опухолей. Meningiomas are by far the most common tumors arising from the meninges. A myriad of aberrant signaling pathways involved with meningioma tumorigenesis, have been discovered. Understanding these disrupted pathways will aid in deciphering the relationship between various genetic changes and their downstream effects on meningioma pathogenesis. An understanding of the genetic and molecular profile of meningioma would provide a valuable first step towards developing more effective treatments for this intracranial tumor. Chromosomes 1, 10, 14, 22, their associated genes, have been linked to meningioma proliferation and progression. It is presumed that through an understanding of these genetic factors, more educated meningioma treatment techniques can be implemented. Future therapies will include combinations of targeted molecular agents including gene therapy, si-RNA mediation, proton therapy, and other approaches as a result of continued progress in the understanding of genetic and biological changes associated with meningiomas.


GYNECOLOGY ◽  
2018 ◽  
Vol 20 (4) ◽  
pp. 9-11 ◽  
Author(s):  
V V Sobolev ◽  
Z A Nevozinskaya ◽  
A G Soboleva ◽  
I M Korsunskaya

The review is devoted to genetic research in cancer of the vulva. In genetic changes, the mutation irreversibly changes the nucleotide sequence of DNA, or the number of copies of chromosomes changes per cell. In epigenetics, the nucleotide sequence remains unchanged, but gene activity is regulated by methylation of DNA or modification of histones. Most of the studies analyzed are devoted to the study of mutations in the TP53 gene. Many studies indicate that somatic mutations are more common in HPV-negative than in HPV-positive patients. Epigenetic studies in the main devoted to hypermethylation. The gene CDKN2A is most often studied in epigenetic terms. For most of the studied genes, hypermethylation occurs more often in squamous cell carcinoma of the vulva than in the precursors.


2018 ◽  
Vol 40 (4) ◽  
pp. 261-267 ◽  
Author(s):  
K Tari ◽  
Z Shamsi ◽  
H Reza Ghafari ◽  
A Atashi ◽  
M Shahjahani ◽  
...  

Chronic lymphocytic leukemia (CLL) is increased proliferation of B-cells with peripheral blood and bone marrow involvement, which is usually observed in older people. Genetic mutations, epigenetic changes and miRs play a role in CLL pathogenesis. Del 11q, del l17q, del 6q, trisomy 12, p53 and IgVH mutations are the most important genetic changes in CLL. Deletion of miR-15a and miR-16a can increase bcl2 gene expression, miR-29 and miR-181 deletions decrease the expression of TCL1, and miR-146a deletion prevents tumor metastasis. Epigenetic changes such as hypo- and hypermethylation, ubiquitination, hypo- and hyperacetylation of gene promoters involved in CLL pathogenesis can also play a role in CLL. Expression of CD38 and ZAP70, presence or absence of mutation in IgVH and P53 mutation are among the factors involved in CLL prognosis. Use of monoclonal antibodies against surface markers of B-cells like anti-CD20 as well as tyrosine kinase inhibitors are the most important therapeutic approaches for CLL.


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