Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria

Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phe...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Silkaitis, Katherine [verfasserIn] Lemos, Bernardo

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Gene expression regulation Drosophila Sexual dimorphisms Sex chromosomes Heterochromatin Y chromosome X chromosome Sex difference

Anmerkung:	© Silkaitis and Lemos; licensee BioMed Central Ltd. 2014

Übergeordnetes Werk:	Enthalten in: Biology of sex differences - London : BioMed Central, 2010, 5(2014), 1 vom: 15. Jan.
Übergeordnetes Werk:	volume:5 ; year:2014 ; number:1 ; day:15 ; month:01

Links:	Volltext

DOI / URN:	10.1186/2042-6410-5-2

Katalog-ID:	SPR031234704

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520			\|a Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases.
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allfields	10.1186/2042-6410-5-2 doi (DE-627)SPR031234704 (SPR)2042-6410-5-2-e DE-627 ger DE-627 rakwb eng Silkaitis, Katherine verfasserin aut Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014 Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. Gene expression regulation (dpeaa)DE-He213 Drosophila (dpeaa)DE-He213 Sexual dimorphisms (dpeaa)DE-He213 Sex chromosomes (dpeaa)DE-He213 Heterochromatin (dpeaa)DE-He213 Y chromosome (dpeaa)DE-He213 X chromosome (dpeaa)DE-He213 Sex difference (dpeaa)DE-He213 Lemos, Bernardo aut Enthalten in Biology of sex differences London : BioMed Central, 2010 5(2014), 1 vom: 15. Jan. (DE-627)642889368 (DE-600)2587352-0 2042-6410 nnns volume:5 year:2014 number:1 day:15 month:01 https://dx.doi.org/10.1186/2042-6410-5-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2086 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2014 1 15 01
spelling	10.1186/2042-6410-5-2 doi (DE-627)SPR031234704 (SPR)2042-6410-5-2-e DE-627 ger DE-627 rakwb eng Silkaitis, Katherine verfasserin aut Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014 Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. Gene expression regulation (dpeaa)DE-He213 Drosophila (dpeaa)DE-He213 Sexual dimorphisms (dpeaa)DE-He213 Sex chromosomes (dpeaa)DE-He213 Heterochromatin (dpeaa)DE-He213 Y chromosome (dpeaa)DE-He213 X chromosome (dpeaa)DE-He213 Sex difference (dpeaa)DE-He213 Lemos, Bernardo aut Enthalten in Biology of sex differences London : BioMed Central, 2010 5(2014), 1 vom: 15. Jan. (DE-627)642889368 (DE-600)2587352-0 2042-6410 nnns volume:5 year:2014 number:1 day:15 month:01 https://dx.doi.org/10.1186/2042-6410-5-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2086 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2014 1 15 01
allfields_unstemmed	10.1186/2042-6410-5-2 doi (DE-627)SPR031234704 (SPR)2042-6410-5-2-e DE-627 ger DE-627 rakwb eng Silkaitis, Katherine verfasserin aut Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014 Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. Gene expression regulation (dpeaa)DE-He213 Drosophila (dpeaa)DE-He213 Sexual dimorphisms (dpeaa)DE-He213 Sex chromosomes (dpeaa)DE-He213 Heterochromatin (dpeaa)DE-He213 Y chromosome (dpeaa)DE-He213 X chromosome (dpeaa)DE-He213 Sex difference (dpeaa)DE-He213 Lemos, Bernardo aut Enthalten in Biology of sex differences London : BioMed Central, 2010 5(2014), 1 vom: 15. Jan. (DE-627)642889368 (DE-600)2587352-0 2042-6410 nnns volume:5 year:2014 number:1 day:15 month:01 https://dx.doi.org/10.1186/2042-6410-5-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2086 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2014 1 15 01
allfieldsGer	10.1186/2042-6410-5-2 doi (DE-627)SPR031234704 (SPR)2042-6410-5-2-e DE-627 ger DE-627 rakwb eng Silkaitis, Katherine verfasserin aut Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014 Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. Gene expression regulation (dpeaa)DE-He213 Drosophila (dpeaa)DE-He213 Sexual dimorphisms (dpeaa)DE-He213 Sex chromosomes (dpeaa)DE-He213 Heterochromatin (dpeaa)DE-He213 Y chromosome (dpeaa)DE-He213 X chromosome (dpeaa)DE-He213 Sex difference (dpeaa)DE-He213 Lemos, Bernardo aut Enthalten in Biology of sex differences London : BioMed Central, 2010 5(2014), 1 vom: 15. Jan. (DE-627)642889368 (DE-600)2587352-0 2042-6410 nnns volume:5 year:2014 number:1 day:15 month:01 https://dx.doi.org/10.1186/2042-6410-5-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2086 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2014 1 15 01
allfieldsSound	10.1186/2042-6410-5-2 doi (DE-627)SPR031234704 (SPR)2042-6410-5-2-e DE-627 ger DE-627 rakwb eng Silkaitis, Katherine verfasserin aut Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014 Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. Gene expression regulation (dpeaa)DE-He213 Drosophila (dpeaa)DE-He213 Sexual dimorphisms (dpeaa)DE-He213 Sex chromosomes (dpeaa)DE-He213 Heterochromatin (dpeaa)DE-He213 Y chromosome (dpeaa)DE-He213 X chromosome (dpeaa)DE-He213 Sex difference (dpeaa)DE-He213 Lemos, Bernardo aut Enthalten in Biology of sex differences London : BioMed Central, 2010 5(2014), 1 vom: 15. Jan. (DE-627)642889368 (DE-600)2587352-0 2042-6410 nnns volume:5 year:2014 number:1 day:15 month:01 https://dx.doi.org/10.1186/2042-6410-5-2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2086 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2014 1 15 01
language	English
source	Enthalten in Biology of sex differences 5(2014), 1 vom: 15. Jan. volume:5 year:2014 number:1 day:15 month:01
sourceStr	Enthalten in Biology of sex differences 5(2014), 1 vom: 15. Jan. volume:5 year:2014 number:1 day:15 month:01
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topic_facet	Gene expression regulation Drosophila Sexual dimorphisms Sex chromosomes Heterochromatin Y chromosome X chromosome Sex difference
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container_title	Biology of sex differences
authorswithroles_txt_mv	Silkaitis, Katherine @@aut@@ Lemos, Bernardo @@aut@@
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author	Silkaitis, Katherine
spellingShingle	Silkaitis, Katherine misc Gene expression regulation misc Drosophila misc Sexual dimorphisms misc Sex chromosomes misc Heterochromatin misc Y chromosome misc X chromosome misc Sex difference Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria
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topic_title	Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria Gene expression regulation (dpeaa)DE-He213 Drosophila (dpeaa)DE-He213 Sexual dimorphisms (dpeaa)DE-He213 Sex chromosomes (dpeaa)DE-He213 Heterochromatin (dpeaa)DE-He213 Y chromosome (dpeaa)DE-He213 X chromosome (dpeaa)DE-He213 Sex difference (dpeaa)DE-He213
topic	misc Gene expression regulation misc Drosophila misc Sexual dimorphisms misc Sex chromosomes misc Heterochromatin misc Y chromosome misc X chromosome misc Sex difference
topic_unstemmed	misc Gene expression regulation misc Drosophila misc Sexual dimorphisms misc Sex chromosomes misc Heterochromatin misc Y chromosome misc X chromosome misc Sex difference
topic_browse	misc Gene expression regulation misc Drosophila misc Sexual dimorphisms misc Sex chromosomes misc Heterochromatin misc Y chromosome misc X chromosome misc Sex difference
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title	Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria
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title_full	Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria
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title_sort	sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria
title_auth	Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria
abstract	Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014
abstractGer	Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014
abstract_unstemmed	Abstract Several autoimmune and neurological diseases exhibit a sex bias, but discerning the causes and mechanisms of these biases has been challenging. Sex differences begin to manifest themselves in early embryonic development, and gonadal differentiation further bifurcates the male and female phenotypes. Even at this early stage, however, there is evidence that males and females respond to environmental stimuli differently, and the divergent phenotypic responses may have consequences later in life. The effect of prenatal nutrient restriction illustrates this point, as adult women exposed to prenatal restrictions exhibited increased risk factors of cardiovascular disease, while men exposed to the same condition did not. Recent research has examined the roles of sex-specific genes, hormones, chromosomes, and the interactions among them in mediating sex-biased phenotypes. Such research has identified testosterone, for example, as a possible protective agent against autoimmune disorders and an XX chromosome complement as a susceptibility factor in murine models of lupus and multiple sclerosis. Sex-biased chromatin is an additional and likely important component. Research suggesting a role for X and Y chromosome heterochromatin in regulating epigenetic states of autosomes has highlighted unorthodox mechanisms of gene regulation. The crosstalk between the Y chromosomes and autosomes may be further mediated by the mitochondria. The organelles have solely maternal transmission and exert differential effects on males and females. Altogether, research supports the notion that the interaction between sex-biased elements might exert novel regulatory functions in the genome and contribute to sex-specific susceptibilities to autoimmune and neurological diseases. © Silkaitis and Lemos; licensee BioMed Central Ltd. 2014
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title_short	Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria
url	https://dx.doi.org/10.1186/2042-6410-5-2
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Sex-biased chromatin and regulatory cross-talk between sex chromosomes, autosomes, and mitochondria

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