scholarly journals Co-evolving wing spots and mating displays are genetically separable traits in Drosophila

2019 ◽  
Author(s):  
Jonathan H. Massey ◽  
Gavin R. Rice ◽  
Anggun Firdaus ◽  
Chi-Yang Chen ◽  
Shu-Dan Yeh ◽  
...  
Keyword(s):  
X Chromosome ◽  
Genetic Basis ◽  
Critical Role ◽  
Genetic Switch ◽  
Behavioral Traits ◽  
Wing Pigmentation ◽  
Physical Linkage ◽  
Sexual Traits ◽  
Male Specific ◽  
And Behavior

AbstractThe evolution of sexual traits often involves correlated changes in morphology and behavior. For example, in Drosophila, divergent mating displays are often accompanied by divergent pigment patterns. To better understand how such traits co-evolve, we investigated the genetic basis of correlated divergence in wing pigmentation and mating display between the sibling species Drosophila elegans and D. gunungcola. Drosophila elegans males have an area of black pigment on their wings known as a wing spot and appear to display this spot to females by extending their wings laterally during courtship. By contrast, D. gunungcola lacks both of these traits. Using Multiplexed Shotgun Genotyping (MSG), we identified a ∼440 kb region on the X chromosome that behaves like a genetic switch controlling the presence or absence of male-specific wing spots. This region includes the candidate gene optomotor-blind (omb), which plays a critical role in patterning the Drosophila wing. The genetic basis of divergent wing display is more complex, with at least two loci on the X chromosome and two loci on autosomes contributing to its evolution. Introgressing the X-linked region affecting wing spot development from D. gunungcola into D. elegans reduced pigmentation in the wing spots but did not affect the wing display, indicating that these are genetically separable traits. Consistent with this observation, broader sampling of wild D. gunungcola populations confirmed the wing spot and wing display are evolving independently: some D. gunungcola males preformed wing displays similar to D. elegans despite lacking wing spots. These data suggest that correlated selection pressures rather than physical linkage or pleiotropy are responsible for the coevolution of these morphological and behavioral traits. They also suggest that the change in morphology evolved prior to the change in behavior.

scholarly journals Genetic Mapping of Climbing and Mimicry: Two Behavioral Traits Degraded During Silkworm Domestication

2020 ◽  
Vol 11 ◽  
Author(s):  
Man Wang ◽  
Yongjian Lin ◽  
Shiyi Zhou ◽  
Yong Cui ◽  
Qili Feng ◽  
...  
Keyword(s):  
Molecular Basis ◽  
Evolutionary Biology ◽  
Genetic Basis ◽  
Bulked Segregant Analysis ◽  
Behavioral Changes ◽  
Behavioral Traits ◽  
Wild Silkworm ◽  
Climbing Ability ◽  
And Behavior ◽  
The Brain

Behavioral changes caused by domestication in animals are an important issue in evolutionary biology. The silkworm, Bombyx mori, is an ideal fully domesticated insect model for studying both convergent domestication and behavior evolution. We explored the genetic basis of climbing for foraging and mimicry, two degraded behaviors during silkworm domestication, in combination of bulked segregant analysis (BSA) and selection sweep screening. One candidate gene, ASNA1, located in the 3–5 Mb on chromosome 19, harboring a specific non-synonymous mutation in domestic silkworm, might be involved in climbing ability. This mutation was under positive selection in Lepidoptera, strongly suggesting its potential function in silkworm domestication. Nine candidate domesticated genes related to mimicry were identified on chromosomes 13, 21, and 27. Most of the candidate domesticated genes were generally expressed at higher levels in the brain of the wild silkworm. This study provides valuable information for deciphering the molecular basis of behavioral changes associated with silkworm domestication.

Assessment of Risk Factors for Severe Coronavirus Disease 2019 among Iranian Patients

2020 ◽  
Keyword(s):  
Risk Factors ◽  
Immune System ◽  
Medical Records ◽  
Critical Role ◽  
Diabetic Patients ◽  
Medication History ◽  
Epidemiological Features ◽  
Hookah Smoking ◽  
And Behavior ◽  
Iranian Patients

Background: The outbreak of Coronavirus Disease 2019 (COVID-19) has led to a major concern for those who are more vulnerable to infections. Objectives: This study aimed to evaluate the most important risk factors for severe COVID-19 pneumonia. Methods: This retrospective study included information on clinical and epidemiological features of 105 patients with severe COVID-19 pneumonia hospitalized in Tajrish Hospital, Tehran, Iran. Initially, the medical records of the patients were investigated, and an interview was conducted based on a pre-prepared checklist to seek information about symptoms, past medical history, medication history, and behavior before hospitalization. Results: Out of 105 participants, 76 (72.5%) cases were male, and 54 (51.4%) patients were older than 54 years old. The majority of the patients (n=18; 17.1%) had both hypertension and diabetes (n=12; 11.4%). Metformin (n=36; 34.3%) was the most used medication amongst the studied patient. In addition, 24 (22.9%) patients were recreational hookah smokers, and the majority (75%) of them were under the age of 46 years old. Eventually, 19 patients were excluded from the study, of whom 11 individuals had diabetes, and 10 cases were using metformin. Conclusion: Apparently, hookah smoking played a critical role in the spread of COVID-19 in Iran and has made younger people more susceptible. In addition to older age, the immunosuppressive effects of Metformin seem to make diabetic patients with an impaired immune system more vulnerable to severe COVID-19 pneumonia. More studies on the immune system of vulnerable individuals by identifying their differences can help to protect them.

scholarly journals Epistatic Control of Non-Mendelian Inheritance in Mouse Interspecific Crosses

Genetics ◽  
1996 ◽  
Vol 143 (4) ◽  
pp. 1739-1752 ◽  
Author(s):  
Xavier Montagutelli ◽  
Rowena Turner ◽  
Joseph H Nadeau
Keyword(s):  
X Chromosome ◽  
Genetic Basis ◽  
Mendelian Inheritance ◽  
The Other ◽  
Interspecific Crosses ◽  
Chromosome 2 ◽  
Mus Spretus ◽  
F1 Hybrid ◽  
Strong Deviation ◽  
Marker Loci

Abstract Strong deviation of allele frequencies from Mendelian inheritance favoring Mus spretus-derived alleles has been described previously for X-linked loci in four mouse interspecific crosses. We reanalyzed data for three of these crosses focusing on the location of the gene(s) controlling deviation on the X chromosome and the genetic basis for incomplete deviation. At least two loci control deviation on the X chromosome, one near Xist (the candidate gene controlling X inactivation) and the other more centromerically located. In all three crosses, strong epistasis was found between loci near Xist and marker loci on the central portion of chromosome 2. The mechanism for this deviation from Mendelian expectations is not yet known but it is probably based on lethality of embryos carrying particular combinations of alleles rather than true segregation distortion during oogenesis in F1 hybrid females.

scholarly journals Absence of X-chromosome dosage compensation in the primordial germ cells of Drosophila embryos

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryoma Ota ◽  
Makoto Hayashi ◽  
Shumpei Morita ◽  
Hiroki Miura ◽  
Satoru Kobayashi
Keyword(s):  
X Chromosome ◽  
Germ Cells ◽  
Dosage Compensation ◽  
Sex Chromosome ◽  
Primordial Germ Cells ◽  
Histone H4 ◽  
X Chromosomes ◽  
Essential Components ◽  
Msl Complex ◽  
Male Specific

AbstractDosage compensation is a mechanism that equalizes sex chromosome gene expression between the sexes. In Drosophila, individuals with two X chromosomes (XX) become female, whereas males have one X chromosome (XY). In males, dosage compensation of the X chromosome in the soma is achieved by five proteins and two non-coding RNAs, which assemble into the male-specific lethal (MSL) complex to upregulate X-linked genes twofold. By contrast, it remains unclear whether dosage compensation occurs in the germline. To address this issue, we performed transcriptome analysis of male and female primordial germ cells (PGCs). We found that the expression levels of X-linked genes were approximately twofold higher in female PGCs than in male PGCs. Acetylation of lysine residue 16 on histone H4 (H4K16ac), which is catalyzed by the MSL complex, was undetectable in these cells. In male PGCs, hyperactivation of X-linked genes and H4K16ac were induced by overexpression of the essential components of the MSL complex, which were expressed at very low levels in PGCs. Together, these findings indicate that failure of MSL complex formation results in the absence of X-chromosome dosage compensation in male PGCs.

scholarly journals Müllerian inhibiting substance contributes to sex-linked biases in the brain and behavior

2009 ◽  
Vol 106 (17) ◽  
pp. 7203-7208 ◽  
Author(s):  
Pei-Yu Wang ◽  
Anna Protheroe ◽  
Andrew N. Clarkson ◽  
Floriane Imhoff ◽  
Kyoko Koishi ◽  
...  
Keyword(s):  
Motor Neurons ◽  
Reproductive Tract ◽  
Behavioral Traits ◽  
Spinal Motor Neurons ◽  
Müllerian Inhibiting Substance ◽  
Males And Females ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Brain ◽  
Mullerian Inhibiting Substance

Many behavioral traits and most brain disorders are common to males and females but are more evident in one sex than the other. The control of these subtle sex-linked biases is largely unstudied and has been presumed to mirror that of the highly dimorphic reproductive nuclei. Sexual dimorphism in the reproductive tract is a product of Müllerian inhibiting substance (MIS), as well as the sex steroids. Males with a genetic deficiency in MIS signaling are sexually males, leading to the presumption that MIS is not a neural regulator. We challenge this presumption by reporting that most immature neurons in mice express the MIS-specific receptor (MISRII) and that male Mis−/− and Misrii−/− mice exhibit subtle feminization of their spinal motor neurons and of their exploratory behavior. Consequently, MIS may be a broad regulator of the subtle sex-linked biases in the nervous system.

The msl-2 dosage compensation gene of Drosophila encodes a putative DNA-binding protein whose expression is sex specifically regulated by Sex-lethal

Development ◽  
1995 ◽  
Vol 121 (10) ◽  
pp. 3245-3258 ◽  
Author(s):  
G.J. Bashaw ◽  
B.S. Baker
Keyword(s):  
Dna Binding ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Ring Finger ◽  
The Other ◽  
Male Specific Lethal ◽  
Alternatively Spliced ◽  
Sex Lethal ◽  
Specific Regulation ◽  
Male Specific

In Drosophila dosage compensation increases the rate of transcription of the male's X chromosome and depends on four autosomal male-specific lethal genes. We have cloned the msl-2 gene and shown that MSL-2 protein is co-localized with the other three MSL proteins at hundreds of sites along the male polytene X chromosome and that this binding requires the other three MSL proteins. msl-2 encodes a protein with a putative DNA-binding domain: the RING finger. MSL-2 protein is not produced in females and sequences in both the 5′ and 3′ UTRs are important for this sex-specific regulation. Furthermore, msl-2 pre-mRNA is alternatively spliced in a Sex-lethal-dependent fashion in its 5′ UTR.

scholarly journals An essential role of acetylcholine-glutamate synergy at habenular synapses in nicotine dependence

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Silke Frahm ◽  
Beatriz Antolin-Fontes ◽  
Andreas Görlich ◽  
Johannes-Friedrich Zander ◽  
Gudrun Ahnert-Hilger ◽  
...  
Keyword(s):  
Synaptic Vesicles ◽  
Critical Role ◽  
Conditioned Reward ◽  
Quantal Size ◽  
Medial Habenula ◽  
Vesicular Transporters ◽  
Circuit Function ◽  
And Behavior ◽  
Presynaptic Facilitation

A great deal of interest has been focused recently on the habenula and its critical role in aversion, negative-reward and drug dependence. Using a conditional mouse model of the ACh-synthesizing enzyme choline acetyltransferase (Chat), we report that local elimination of acetylcholine (ACh) in medial habenula (MHb) neurons alters glutamate corelease and presynaptic facilitation. Electron microscopy and immuno-isolation analyses revealed colocalization of ACh and glutamate vesicular transporters in synaptic vesicles (SVs) in the central IPN. Glutamate reuptake in SVs prepared from the IPN was increased by ACh, indicating vesicular synergy. Mice lacking CHAT in habenular neurons were insensitive to nicotine-conditioned reward and withdrawal. These data demonstrate that ACh controls the quantal size and release frequency of glutamate at habenular synapses, and suggest that the synergistic functions of ACh and glutamate may be generally important for modulation of cholinergic circuit function and behavior.

scholarly journals Fruitless Represses robo1 Transcription to Shape Male-Specific Neural Morphology and Behavior in Drosophila

2016 ◽  
Vol 26 (12) ◽  
pp. 1532-1542 ◽  
Author(s):  
Hiroki Ito ◽  
Kosei Sato ◽  
Shu Kondo ◽  
Ryu Ueda ◽  
Daisuke Yamamoto
Keyword(s):  
Male Specific ◽  
And Behavior

Drosophila Male-Specific Lethal 2 Protein Controls Sex-Specific Expression of the roX Genes

Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1825-1832 ◽  
Author(s):  
Barbara P Rattner ◽  
Victoria H Meller
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
X Chromosome ◽  
Specific Expression ◽  
Linked Gene ◽  
Male And Female ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific ◽  
Rox Rna

Abstract The MSL complex of Drosophila upregulates transcription of the male X chromosome, equalizing male and female X-linked gene expression. Five male-specific lethal proteins and at least one of the two noncoding roX RNAs are essential for this process. The roX RNAs are required for the localization of MSL complexes to the X chromosome. Although the mechanisms directing targeting remain speculative, the ratio of MSL protein to roX RNA influences localization of the complex. We examine the transcriptional regulation of the roX genes and show that MSL2 controls male-specific roX expression in the absence of any other MSL protein. We propose that this mechanism maintains a stable MSL/roX ratio that is favorable for localization of the complex to the X chromosome.

scholarly journals Cerebellar ataxia, neuropathy, hearing loss, and intellectual disability due to AIFM1 mutation

2020 ◽  
Vol 6 (3) ◽  
pp. e420 ◽  
Author(s):  
Massimo Pandolfo ◽  
Myriam Rai ◽  
Gauthier Remiche ◽  
Laurence Desmyter ◽  
Isabelle Vandernoot
Keyword(s):  
Hearing Loss ◽  
Intellectual Disability ◽  
Cerebellar Ataxia ◽  
X Chromosome ◽  
Behavior Disorder ◽  
X Chromosome Inactivation ◽  
Chromosome Inactivation ◽  
Behavioral Disorder ◽  
Maternal Uncle ◽  
And Behavior

ObjectiveTo describe the clinical and molecular genetic findings in a family segregating a novel mutation in the AIFM1 gene on the X chromosome.MethodsWe studied the clinical features and performed brain MRI scans, nerve conduction studies, audiometry, cognitive testing, and clinical exome sequencing (CES) in the proband, his mother, and maternal uncle. We used in silico tools, X chromosome inactivation assessment, and Western blot analysis to predict the consequences of an AIFM1 variant identified by CES and demonstrate its pathogenicity.ResultsThe proband and his maternal uncle presented with childhood-onset nonprogressive cerebellar ataxia, hearing loss, intellectual disability (ID), peripheral neuropathy, and mood and behavioral disorder. The proband's mother had mild cerebellar ataxia, ID, and mood and behavior disorder, but no neuropathy or hearing loss. The 3 subjects shared a variant (c.1195G>A; p.Gly399Ser) in exon 12 of the AIFM1 gene, which is not reported in the exome/genome sequence databases, affecting a critical amino acid for protein function involved in NAD(H) binding and predicted to be pathogenic with very high probability by variant analysis programs. X chromosome inactivation was highly skewed in the proband's mother. The mutation did not cause quantitative changes in protein abundance.ConclusionsOur report extends the molecular and phenotypic spectrum of AIFM1 mutations. Specific findings include limited progression of neurologic abnormalities after the first decade and the coexistence of mood and behavior disorder. This family also shows the confounding effect on the phenotype of nongenetic factors, such as alcohol and drug use and side effects of medication.

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