scholarly journals Male-Specific Fruitless Isoforms Target Neurodevelopmental Genes to Specify a Sexually Dimorphic Nervous System

2014 ◽  
Vol 24 (3) ◽  
pp. 229-241 ◽  
Author(s):  
Megan C. Neville ◽  
Tetsuya Nojima ◽  
Elizabeth Ashley ◽  
Darren J. Parker ◽  
John Walker ◽  
...  
Keyword(s):  
Nervous System ◽  
Sexually Dimorphic ◽  
Male Specific

scholarly journals Timing mechanism of sexually dimorphic nervous system differentiation

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Laura Pereira ◽  
Florian Aeschimann ◽  
Chen Wang ◽  
Hannah Lawson ◽  
Esther Serrano-Saiz ◽  
...  
Keyword(s):  
Nervous System ◽  
Transcription Factors ◽  
Molecular Mechanisms ◽  
Sex Chromosome ◽  
Sexually Dimorphic ◽  
Neuron Type ◽  
Chromosome Configuration ◽  
Opposite Sex ◽  
Male Specific ◽  
Spatial Specificity

The molecular mechanisms that control the timing of sexual differentiation in the brain are poorly understood. We found that the timing of sexually dimorphic differentiation of postmitotic, sex-shared neurons in the nervous system of the Caenorhabditis elegans male is controlled by the temporally regulated miRNA let-7 and its target lin-41, a translational regulator. lin-41 acts through lin-29a, an isoform of a conserved Zn finger transcription factor, expressed in a subset of sex-shared neurons only in the male. Ectopic lin-29a is sufficient to impose male-specific features at earlier stages of development and in the opposite sex. The temporal, sexual and spatial specificity of lin-29a expression is controlled intersectionally through the lin-28/let-7/lin-41 heterochronic pathway, sex chromosome configuration and neuron-type-specific terminal selector transcription factors. Two Doublesex-like transcription factors represent additional sex- and neuron-type specific targets of LIN-41 and are regulated in a similar intersectional manner.

scholarly journals Timing mechanism of sexually dimorphic nervous system differentiation

2018 ◽  
Author(s):  
Laura Pereira ◽  
Florian Aeschimann ◽  
Chen Wang ◽  
Hannah Lawson ◽  
Esther Serrano-Saiz ◽  
...  
Keyword(s):  
Nervous System ◽  
Transcription Factors ◽  
Sexual Maturation ◽  
Sexual Differentiation ◽  
Rna Binding ◽  
Receptor Expression ◽  
Sexually Dimorphic ◽  
Neuron Type ◽  
C Elegans ◽  
Male Specific

ABSTRACTIn all animals, sexual differentiation of somatic tissue is precisely timed, yet the molecular mechanisms that control the timing of sexual differentiation, particularly in the brain, are poorly understood. We have used sexually dimorphic molecular, anatomical and behavioral features of the C. elegans nervous system to decipher a regulatory pathway that controls the precise timing of sexual differentiation. We find that the sexually dimorphic differentiation of postmitotic neurons in the male nervous system is abrogated in animals that carry a mutation in the miRNA let-7 and prematurely executed in animals either lacking the let-7 inhibitor lin-28, or the direct let-7 target lin-41, an RNA-binding, posttranscriptional regulator. We show that an isoform of a phylogenetically conserved transcription factor, lin-29a, is a critical target of LIN-41 in controlling sexual maturation of sex-shared neurons. lin-29a is expressed in a male-specific manner in a subset of sex-shared neurons at the onset of sexual maturation. lin-29a acts cell-autonomously in these neurons to control the expression of sexually dimorphic neurotransmitter switches, sensory receptor expression, neurite anatomy and connectivity, and locomotor behavior. lin-29a is not only required but also sufficient to impose male-specific features at earlier stages of development and in the opposite sex. The temporal, sexual and spatial specificity of lin-29a expression is controlled intersectionally through the lin-28/let-7/lin-41 heterochronic pathway, sex chromosome configuration and neuron type-specific terminal selector transcription factors. Two Doublesex-like transcription factors represent additional neuron-type specific targets of LIN-41 and are regulated in a similar intersectional manner, indicating the existence of modular outputs downstream of the heterochronic pathway. In conclusion, we have provided insights into the molecular logic of the timing of sexual differentiation in the C. elegans nervous system. Remarkably, the lin28/let7 axis also controls the timing of sexual differentiation in mice and humans thereby hinting toward a striking universality of the control mechanisms of sexual differentiation.

scholarly journals Physiopathological Role of Neuroactive Steroids in the Peripheral Nervous System

2020 ◽  
Vol 21 (23) ◽  
pp. 9000
Author(s):  
Eva Falvo ◽  
Silvia Diviccaro ◽  
Roberto Cosimo Melcangi ◽  
Silvia Giatti
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Experimental Models ◽  
Neuroactive Steroids ◽  
Physiological Status ◽  
Sexually Dimorphic ◽  
Protective Effects ◽  
Traumatic Injuries ◽  
High Prevalence

Peripheral neuropathy (PN) refers to many conditions involving damage to the peripheral nervous system (PNS). Usually, PN causes weakness, numbness and pain and is the result of traumatic injuries, infections, metabolic problems, inherited causes, or exposure to chemicals. Despite the high prevalence of PN, available treatments are still unsatisfactory. Neuroactive steroids (i.e., steroid hormones synthesized by peripheral glands as well as steroids directly synthesized in the nervous system) represent important physiological regulators of PNS functionality. Data obtained so far and here discussed, indeed show that in several experimental models of PN the levels of neuroactive steroids are affected by the pathology and that treatment with these molecules is able to exert protective effects on several PN features, including neuropathic pain. Of note, the observations that neuroactive steroid levels are sexually dimorphic not only in physiological status but also in PN, associated with the finding that PN show sex dimorphic manifestations, may suggest the possibility of a sex specific therapy based on neuroactive steroids.

scholarly journals Nixalone is sufficient to convert femaleAedes aegyptiinto fertile males andmyo-sexis needed for male flight

2020 ◽  
Vol 117 (30) ◽  
pp. 17702-17709 ◽  
Author(s):  
Azadeh Aryan ◽  
Michelle A. E. Anderson ◽  
James K. Biedler ◽  
Yumin Qi ◽  
Justin M. Overcash ◽  
...  
Keyword(s):  
Mosquito Control ◽  
Control Strategies ◽  
Reproductive Organs ◽  
Dominant Male ◽  
Chain Gene ◽  
Sexually Dimorphic ◽  
Wild Type ◽  
Transgenic Lines ◽  
Male Sex ◽  
Male Specific

A dominant male-determining locus (M-locus) establishes the male sex (M/m) in the yellow fever mosquito,Aedes aegypti.Nix, a gene in the M-locus, was shown to be a male-determining factor (M factor) as somatic knockout ofNixled to feminized males (M/m) while transient expression ofNixresulted in partially masculinized females (m/m), with male reproductive organs but retained female antennae. It was not clear whether any of the other 29 genes in the 1.3-Mb M-locus are also needed for complete sex-conversion. Here, we report the generation of multiple transgenic lines that expressNixunder the control of its own promoter. Genetic and molecular analyses of these lines provided insights unattainable from previous transient experiments. We show that theNixtransgene alone, in the absence of the M-locus, was sufficient to convert females into males with all male-specific sexually dimorphic features and male-like gene expression. The converted m/m males are flightless, unable to perform the nuptial flight required for mating. However, they were able to father sex-converted progeny when presented with cold-anesthetized wild-type females. We show thatmyo-sex, a myosin heavy-chain gene also in the M-locus, was required for male flight as knockout ofmyo-sexrendered wild-type males flightless. We also show thatNix-mediated female-to-male conversion was 100% penetrant and stable over many generations. Therefore,Nixhas great potential for developing mosquito control strategies to reduce vector populations by female-to-male sex conversion, or to aid in a sterile insect technique that requires releasing only non-biting males.

scholarly journals NANOS2 suppresses the cell cycle by repressing mTORC1 activators in embryonic male germ cells

2020 ◽  
Author(s):  
Ryuki Shimada ◽  
Hiroko Koike ◽  
Takamasa Hirano ◽  
Yumiko Saga
Keyword(s):  
Cell Cycle ◽  
Germ Cell ◽  
Germ Cells ◽  
Rna Binding ◽  
Initial Step ◽  
Sexually Dimorphic ◽  
Wild Type ◽  
Male Germ Cells ◽  
Cycle Arrest ◽  
Male Specific

AbstractDuring murine germ cell development, male germ cells enter the mitotically arrested G0 stage, which is an initial step of sexually dimorphic differentiation. The male specific RNA-binding protein NANOS2 has a key role in suppressing the cell cycle in germ cells. However, the detailed mechanism of how NANOS2 regulates the cell cycle remains unclear. Using single-cell RNA sequencing (scRNA-seq), we extracted the cell cycle state of each germ cell in wild-type and Nanos2-KO testes, and revealed that Nanos2 expression starts in mitotic cells and induces mitotic arrest. We also found that NANOS2 and p38 MAPK work in parallel to regulate the cell cycle, suggesting that several different cascades are involved in the induction of cell cycle arrest. Furthermore, we identified Rheb, a regulator of mTORC1, and Ptma as possible targets of NANOS2. We propose that the repression of the cell cycle is a primary function of NANOS2 and that it is mediated via the suppression of mTORC1 activity by repressing Rheb in a post-transcriptional manner.

scholarly journals Direct glia-to-neuron transdifferentiation gives rise to a pair of male-specific neurons that ensure nimble male mating

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Laura Molina-García ◽  
Carla Lloret-Fernández ◽  
Steven J Cook ◽  
Byunghyuk Kim ◽  
Rachel C Bonnington ◽  
...  
Keyword(s):  
Cell Fate ◽  
Molecular Mechanisms ◽  
Male Mating ◽  
Sexually Dimorphic ◽  
Innate Behaviour ◽  
One Step ◽  
Males And Females ◽  
Direct Transdifferentiation ◽  
Male Specific ◽  
Mating Sequence

Sexually dimorphic behaviours require underlying differences in the nervous system between males and females. The extent to which nervous systems are sexually dimorphic and the cellular and molecular mechanisms that regulate these differences are only beginning to be understood. We reveal here a novel mechanism by which male-specific neurons are generated in Caenorhabditis elegans through the direct transdifferentiation of sex-shared glial cells. This glia-to-neuron cell fate switch occurs during male sexual maturation under the cell-autonomous control of the sex-determination pathway. We show that the neurons generated are cholinergic, peptidergic, and ciliated putative proprioceptors which integrate into male-specific circuits for copulation. These neurons ensure coordinated backward movement along the mate’s body during mating. One step of the mating sequence regulated by these neurons is an alternative readjustment movement performed when intromission becomes difficult to achieve. Our findings reveal programmed transdifferentiation as a developmental mechanism underlying flexibility in innate behaviour.

Sign in / Sign up

Export Citation Format

Share Document