Transgressive segregation and maternal genetic effects of non–target site fluazifop-P-butyl tolerance in Zoysia spp.

Weed Science ◽  
2019 ◽  
Vol 67 (05) ◽  
pp. 504-509
Author(s):  
Wenwen Liu ◽  
Kevin E. Kenworthy ◽  
Gregory E. MacDonald ◽  
J. Bryan Unruh ◽  
Laurie E. Trenholm ◽  
...  

AbstractZoysia germplasm exhibit different levels of sensitivity to fluazifop-P-butyl, but the genetic factors responsible for such differences are unknown. Segregation patterns of the fluazifop-P-butyl tolerance trait were studied under greenhouse conditions. In total, 244 F1 lines were generated from multiple crosses between the tolerant line 5337-2 (non–target site tolerance) and three more-sensitive lines (123, 252, and 5330-23). Progeny segregation showed that fluazifop-P-butyl tolerance within zoysiagrass (Zoysia spp.) is expressed as a quantitative trait with a wide range of intermediate phenotypes between parental phenotypes. Transgressive segregation was extensive and largely favored susceptibility in most families, but was especially evident for 5337-2 × 123 and 5337-2 × 5330-23. The segregation patterns for biomass reduction and percent injury were different within reciprocal crosses and among three different family crosses. Reciprocal effects were observed in growth reduction for 5337-2 × 5330-23, in percent injury at 3 wk after the treatment (WAT), and for 5337-2 × 252 at 6 WAT. This indicated that fluazifop-P-butyl tolerance was not completely controlled by nuclear genetic factors in 5337-2 and maternal/cytoplasmic inheritance was also partially responsible. These results suggested that fluazifop-P-butyl tolerance may be attributed to multiple genetic mechanisms, which could present a challenge for future breeding efforts because of the difficulty of fixing multiple traits within a breeding population.

2021 ◽  
Vol 11 (3) ◽  
pp. 1-2
Author(s):  
Fernando Russo Costa do Bomfim

Genetics is specifically responsible for several pathologies or, at the least, it is associated with a wide range of them, either as a primary causal agent (congenital genetic diseases) or secondary, being a factor within several possible for a given disease. One of the most critical genetic concepts is developed from the phenotype, equivalent to the genotype associated with the environment. In other words, for a condition to manifest itself, cancer, for example, we need a genetic alteration within the environment, which somehow influences carcinogenesis from stochastic or induced interactions. Cancer cases are approximately 80% and 90% associated with external causes, and environmental changes are mainly motivated by human actions, habits, and behavior, leading to an increased risk of different types of cancer. These changes lead to the formation of a cycle since man promotes environmental changes, leading to genetic modifications responsible for 10-20% of cancer formation. Although the percentage seems not to be significant, we have, in fact, several genetic mechanisms that will lead to the emergence of the most diverse types of cancer, including polymorphisms, mutations, oxidative stress, oncogenes, and genes that regulate the cell cycle, including apoptosis.


2006 ◽  
Vol 9 (6) ◽  
pp. 811-816 ◽  
Author(s):  
Chizuru Shikishima ◽  
Juko Ando ◽  
Yutaka Ono ◽  
Tatsushi Toda ◽  
Kimio Yoshimura

AbstractSince established in 1998, the Keio Twin Project (KTP) has been dedicated to investigating genetic and environmental sources contributing to human psychological traits in adolescence and young adulthood. A population-based twin registry was constructed by the KTP through the use of official residential records in the Tokyo area, and to date requests to participate in our research have generated 1040 pairs of twins and triplets of age 14 to 30, forming one of the largest twin registries in Asia. Our comprehensive datasets, obtained through questionnaires, performance tests, and physical measurements, cover a wide range of human traits: personality, psychiatry, mental health, sociality, cognition, and physical index. Demographic variables and environment of upbringing are also sought by twins and by some parents. This extensive information allows us to clarify the genetic and environmental overlap across multiple traits as well as specificities unique to single traits. Adding an evolutionary psychology perspective to the behavior genetics framework is currently being attempted in order to develop a grand theory of human genetics.


2021 ◽  
Vol 23 ◽  
Author(s):  
Pei He ◽  
Rong- Rong Cao ◽  
Fei- Yan Deng ◽  
Shu- Feng Lei

Background: Immune and skeletal systems physiologically and pathologically interact with each other. The immune and skeletal diseases may share potential pleiotropic genetics factors, but the shared specific genes are largely unknown Objective: This study aimed to investigate the overlapping genetic factors between multiple diseases (including rheumatoid arthritis (RA), psoriasis, osteoporosis, osteoarthritis, sarcopenia and fracture) Methods: The canonical correlation analysis (metaCCA) approach was used to identify the shared genes for six diseases by integrating genome-wide association study (GWAS)-derived summary statistics. Versatile Gene-based Association Study (VEGAS2) method was further applied to refine and validate the putative pleiotropic genes identified by metaCCA. Results: About 157 (p<8.19E-6), 319 (p<3.90E-6) and 77 (p<9.72E-6) potential pleiotropic genes were identified shared by two immune disease, four skeletal diseases, and all of the six diseases, respectively. The top three significant putative pleiotropic genes shared by both immune and skeletal diseases, including HLA-B, TSBP1 and TSBP1-AS1 (p<E-300) were located in the major histocompatibility complex (MHC) region. Nineteen of 77 putative pleiotropic genes identified by metaCCA analysis were associated with at least one disease in the VEGAS2 analysis. Specifically, majority (18) of these 19 putative validated pleiotropic genes were associated with RA. Conclusion: The metaCCA method identified some pleiotropic genes shared by the immune and skeletal diseases. These findings help to improve our understanding of the shared genetic mechanisms and signaling pathways underlying immune and skeletal diseases.


Demography ◽  
2021 ◽  
Author(s):  
Zachary Van Winkle ◽  
Dalton Conley

Abstract Sequence analysis is an established method used to study the complexity of family life courses. Although individual and societal characteristics have been linked with the complexity of family trajectories, social scientists have neglected the potential role of genetic factors in explaining variation in family transitions and events across the life course. We estimate the genetic contribution to sequence complexity and a wide range of family demographic behaviors using genomic relatedness–based, restricted maximum likelihood models with data from the U.S. Health and Retirement Study. This innovative methodological approach allows us to provide the first estimates of the heritability of composite life course outcomes—that is, sequence complexity. We demonstrate that a number of family demographic indicators (e.g., the age at first birth and first marriage) are heritable and provide evidence that composite metrics can be influenced by genetic factors. For example, our results show that 11% of the total variation in the complexity of differentiated family sequences is attributable to genetic influences. Moreover, we test whether this genetic contribution varies by social environment as indexed by birth cohort over a period of rapid changes in family norms during the twentieth century. Interestingly, we find evidence that the complexity of fertility and differentiated family trajectories decreased across cohorts, but we find no evidence that the heritability of the complexity of partnership trajectories changed across cohorts. Therefore, our results do not substantiate claims that lower normative constraints on family demographic behavior increase the role of genes.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S925-S925
Author(s):  
Chia-Ling Kuo ◽  
Ziwei Pan ◽  
Luke C Pilling ◽  
George A Kuchel ◽  
David Melzer

Abstract Genetic variants associated with multiple traits are potential targets to delay aging. Drugs supported by genetic evidence are twice as likely to succeed in human trials. Single nucleotide polymorphisms (SNPs) in the ABO gene were reported by genome-wide associations studies, associated with breast cancer, coronary artery disease, stroke, and type II diabetes. To evaluate the potential of ABO gene as a target for aging intervention, we conducted a phenome-wide association study (PheWAS) to associate the genotype-derived blood types (based on two SNPs in the ABO gene) with a wide range of aging-related outcomes. The genotype-derived blood type distribution (41% A, 9% B, 3% AB, and 47% O) is similar to that reported by the UK National Health Service (39% A, 10% B, 3% AB, and 48% O). The blood type was not associated with parental lifespan or extreme parental longevity. Non-O types had modestly lower risk of hypertension than O type but higher risk of type II diabetes and pancreatic cancer (e.g., OR= 1.37, 95% CI: 1.17 to 1.59 comparing A to O). Additionally, “A" type had modestly higher risk of breast cancer than other types. “A” allele (in A or AB type) was associated with lower heel bone mineral density, alkaline phosphatase (e.g., 0.41 standard deviation lower in A than that in O, 95% CI: -0.42 to -0.40), and hemoglobin concentration, but higher HbA1c, direct LDL, and cholesterol. Blood types with A allele(s) are less favored than other blood types, which however are adversely associated with some aging traits.


Zootaxa ◽  
2011 ◽  
Vol 3130 (1) ◽  
pp. 30 ◽  
Author(s):  
YUVINKA GARECA ◽  
PATRICK BLANDIN

The geographical distribution of Morpho helenor (Cramer) in Bolivia is mapped from the study of specimens preserved in Bolivian and foreign collections, and from recent field studies in various ecoregions. One subspecies, M. h. theodorus Fruhstorfer, inhabits Amazonian moist forests in the western and northern parts of the country. Another subspecies, M. h. coelestis Butler, is common in moist cloud forests (Bolivian Yungas), but also occurs to the North and North-East. We describe a new subspecies, M. h. prometa ssp. nov., from Southern Andean Yungas. Transition zones between theodorus and coelestis are highlighted, where specimens exhibiting intermediate phenotypes were collected. The pattern of geographic transition from M. h. coelestis to M. h. prometa needs to be documented. M. h. prometa inhabits sub-humid, semideciduous forests, whereas M. h. theodorus and M. h. coelestis live in rainforests. M. h. coelestis populations are found from less than 100 m to more than 1600 m a.s.l.; M. h. theodorus has been collected at more than 1000 m a.s.l.; and M. h. prometa between 500 m and 1400 m a.s.l.. Therefore, Bolivian M. helenor populations are distributed throughout a wide range of ecological contexts: we discuss the habitat plasticity of the species in light of available knowledge of its geographical distribution and habitats in the Neotropical Region.


2020 ◽  
Vol 09 (02) ◽  
pp. 077-086
Author(s):  
Maria Kostara ◽  
Vasiliki Chondrou ◽  
Argyro Sgourou ◽  
Konstantinos Douros ◽  
Sophia Tsabouri

AbstractFood allergy (FA) is a growing health problem that affects ∼8% of the children worldwide. Although the prevalence of FA is increasing, the underlying genetic mechanisms responsible for the onset of this immune disorder are not yet clarified. Genetic factors seem to play a leading role in the development of FA, though interaction with environmental factors cannot be excluded. The broader network of genetic loci mediating the risk of this complex disorder remains to be identified. The human leucocyte antigen (HLA) has been associated with various immune disorders, including FA. This review aims to unravel the potential associations between HLA gene functions and the manifestation and outcome of FA disorders. Exploring new aspects of FA development with the perspective to improve our understanding of the multifaceted etiology and the complex biological mechanisms involved in FA is essential.


2006 ◽  
Vol 7 (10) ◽  
pp. 818-827 ◽  
Author(s):  
Andreas Meyer-Lindenberg ◽  
Daniel R. Weinberger

2012 ◽  
Vol 109 (38) ◽  
pp. 15206-15211 ◽  
Author(s):  
Nicole Joußen ◽  
Sara Agnolet ◽  
Sybille Lorenz ◽  
Sebastian E. Schöne ◽  
Renate Ellinger ◽  
...  

Worldwide, increasing numbers of insects have evolved resistance to a wide range of pesticides, which hampers their control in the field and, therefore, threatens agriculture. Members of the carboxylesterase and cytochrome P450 monooxygenase superfamilies are prominent candidates to confer metabolic resistance to pyrethroid insecticides. Both carboxylesterases and P450 enzymes have been shown to be involved in pyrethroid resistance in Australian Helicoverpa armigera, the noctuid species possessing by far the most reported resistance cases worldwide. However, specific enzymes responsible for pyrethroid resistance in field populations of this species have not yet been identified. Here, we show that the resistance toward fenvalerate in an Australian strain of H. armigera is due to a unique P450 enzyme, CYP337B3, which arose from unequal crossing-over between two parental P450 genes, resulting in a chimeric enzyme. CYP337B3 is capable of metabolizing fenvalerate into 4′-hydroxyfenvalerate, which exhibits no toxic effect on susceptible larvae; enzymes from the parental P450 genes showed no detectable fenvalerate metabolism. Furthermore, a polymorphic H. armigera strain could be bred into a susceptible line possessing the parental genes CYP337B1 and CYP337B2 and a resistant line possessing only CYP337B3. The exclusive presence of CYP337B3 in resistant insects of this strain confers a 42-fold resistance to fenvalerate. Thus, in addition to previously documented genetic mechanisms of resistance, recombination can also generate selectively advantageous variants, such as this chimeric P450 enzyme with an altered substrate specificity leading to a potent resistance mechanism.


2014 ◽  
Author(s):  
Xia Shen ◽  
Jennifer De Jonge ◽  
Simon Forsberg ◽  
Mats Pettersson ◽  
Zheya Sheng ◽  
...  

As Arabidopsis thaliana has colonized a wide range of habitats across the world it is an attractive model for studying the genetic mechanisms underlying environmental adaptation. Here, we used public data from two collections of A. thaliana accessions to associate genetic variability at individual loci with differences in climates at the sampling sites. We use a novel method to screen the genome for plastic alleles that tolerate a broader climate range than the major allele. This approach reduces confounding with population structure and increases power compared to standard genome-wide association methods. Sixteen novel loci were found, including an association between Chromomethylase 2 (CMT2) and temperature seasonality where the genome-wide CHH methylation was different for the group of accessions carrying the plastic allele. Cmt2 mutants were shown to be more tolerant to heat-stress, suggesting genetic regulation of epigenetic modifications as a likely mechanism underlying natural adaptation to variable temperatures, potentially through differential allelic plasticity to temperature-stress.


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