Proteins in urine scent marks of male house mice extend the longevity of olfactory signals

Hurst, Jane L.; Robertson, Duncan H. L.; Tolladay, Ursula; Beynon, Robert J.

doi:10.1006/anbe.1997.0650

Cited by 225 publications

(172 citation statements)

References 33 publications

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“…Except for the case of gel permeation chromatography, all other methods consistently confirmed that compounds with low molecular weight were responsible for the discriminative MHC signals. Although the bioassay-active fraction obtained using gel permeation chromatography was the protein fraction, it is probable that volatiles were the active compounds because most of the protein-the major urinary proteins (MUPs)-strongly sequester volatile compounds and release them slowly (Bacchini et al 1992;Hurst et al 1998). In addition, the sensor mice were not allowed to contact the samples and therefore it is probable that only airborne compounds released from the protein fraction were delivered to the Y-maze for the bioassay.…”

Section: Chemical Investigations Of Mhc Odourtype In Micementioning

confidence: 99%

“…Behavioural differences among individuals could result in different patterns of food and water consumption, and hence urination frequencies, which could impact proportions of volatiles. Individual variation in volatile profiles may also be affected by variation in MUP content, which may change volatile profiles since MUPs retain volatile compounds and release them slowly (Bacchini et al 1992;Hurst et al 1998). …”

Section: Why Do Published Studies Show Little Agreement On the Identimentioning

confidence: 99%

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In search of the chemical basis for MHC odourtypes

et al. 2010

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Mice can discriminate between chemosignals of individuals based solely on genetic differences confined to the major histocompatibility complex (MHC). Two different sets of compounds have been suggested: volatile compounds and non-volatile peptides. Here, we focus on volatiles and review a number of publications that have identified MHC-regulated compounds in inbred laboratory mice. Surprisingly, there is little agreement among different studies as to the identity of these compounds. One recent approach to specifying MHC-regulated compounds is to study volatile urinary profiles in mouse strains with varying MHC types, genetic backgrounds and different diets. An unexpected finding from these studies is that the concentrations of numerous compounds are influenced by interactions among these variables. As a result, only a few compounds can be identified that are consistently regulated by MHC variation alone. Nevertheless, since trained animals are readily able to discriminate the MHC differences, it is apparent that chemical studies are somehow missing important information underlying mouse recognition of MHC odourtypes. To make progress in this area, we propose a focus on the search for behaviourally relevant odourants rather than a random search for volatiles that are regulated by MHC variation. Furthermore, there is a need to consider a 'combinatorial odour recognition' code whereby patterns of volatile metabolites (the basis for odours) specify MHC odourtypes.

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Section: Chemical Investigations Of Mhc Odourtype In Micementioning

confidence: 99%

Section: Why Do Published Studies Show Little Agreement On the Identimentioning

confidence: 99%

In search of the chemical basis for MHC odourtypes

et al. 2010

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“…Males excrete in their urine extremely large concentrations of major urinary proteins (MUPs). These MUPs have a number of roles in sexual signaling, including binding and releasing volatile odorants slowly over time (21) and inducing female attraction and memory of scent (22). Experimentally increasing the concentration of these proteins in urine increases the attractiveness of male scent to females (23), indicating that any changes in MUP concentration with oxidative stress are likely to influence male attractiveness.…”

Section: Resultsmentioning

confidence: 99%

Superoxide dismutase deficiency impairs olfactory sexual signaling and alters bioenergetic function in mice

Garratt¹,

Pichaud²,

Glaros

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Oxidative stress (an overproduction of reactive oxygen species in relation to defense mechanisms) may restrict investment in life history traits, such as growth, reproduction, lifespan, and the production of sexual signals to attract mates. The constraint on sexual signaling by oxidative stress is of particular interest because it has been proposed as a mechanism ensuring that only good-quality males produce the most attractive sexual signals. Despite these predictions, evidence supporting this theory is, at best, equivocal. We used a superoxide dismutase knockout mouse to demonstrate that oxidative stress directly impairs investment in morphological (preputial glands) and molecular (major urinary proteins) components of olfactory signaling essential for mate attraction. By maintaining males in a much more competitive environment than usual for mouse laboratory experiments, we also revealed a range of phenotypes of superoxide dismutase deficiency not observed in previous studies of this mouse model. This range included impaired bioenergetic function, which was undetectable in the control environment of this study. We urge further examination of model organisms in seminatural conditions and more competitive laboratory environments, as important phenotypes can be exposed under these more demanding conditions.L ife history theory is based on the premise that physiological constraints limit investment in life history components. These constraints are expected to generate the negative correlations commonly observed between these traits on an interspecies level (1). Within species, individuals also differ in their capacity to invest in different traits (2), although the physiological causes of this variation remain largely elusive.Oxidative stress occurs as a consequence of an overproduction of reactive oxygen species (ROS) in relation to defense mechanisms (3). Because ROS are produced as a by-product of oxidative phosphorylation, investment in energetically demanding life history traits has been predicted to increase oxidative stress, which may then constrain investment in other areas (4, 5). Ecological research in wild animals has provided correlative evidence for a link between oxidative stress and investment in traits, such as growth (6), reproduction (7,8), and lifespan (7). Early evidence linking oxidative stress to variation in lifespan within (9) and between species (10) led to the development of genetically modified antioxidant enzyme knockout animals, allowing precise tests of the effects of these pathways on lifespan under controlled laboratory conditions (11). These tests concluded that oxidative stress does not play a major role in governing the lifespan of laboratory animals (11).As in the case of lifespan, sexual signals show considerable among-individual variation and can correlate with oxidative stress. Sexual signals are often condition-dependent in expression, such that only good-quality signalers express the largest or most elaborate sexual signals (12). These signaling systems only evolve and rem...

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“…MUPs are a family proteins of ϳ20 kDa that are expressed in and secreted by the liver. There are 35-40 MUP genes and pseudogenes in mice (38,39), and the encoded MUP proteins are thought to contribute to scent marking of territories (40). About 3-fold higher levels of MUPs are excreted in male compared with female mouse urine, and the high level expression of some of these genes is induced by pulsatile GH and suppressed by GH administered continuously.…”

Section: Figmentioning

confidence: 99%

STAT5b-deficient Mice Are Growth Hormone Pulse-resistant

Davey¹,

Park²,

Grattan³

et al. 1999

Journal of Biological Chemistry

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The signal transducer and transcriptional activator STAT5b is required to maintain the adult male pattern of liver gene expression and whole body pubertal growth rates, as demonstrated by the loss of these growth hormone (GH) pulse-dependent responses in mice with a targeted disruption of the STAT5b gene. The present study investigates whether these phenotypes of STAT5b-deficient mice result from impaired intracellular GH signaling associated with a loss of GH pulse responsiveness, as contrasted with a feminization of the pituitary GH secretory profile leading to the observed feminization of body growth and liver gene expression. Pulsatile GH replacement in hypophysectomized mice stimulated body weight gain in wild-type but not in STAT5b-deficient mice. Expression of the male-specific liver P450 enzyme CYP2D9, which is reduced to female levels in hypophysectomized male mice, was restored to male levels by GH pulse replacement in wild-type but not in STAT5b-deficient mice. Similarly, a female-specific liver CYP2B P450 enzyme that was up-regulated to female levels following hypophysectomy of males was suppressed to normal basal male levels by GH pulses only in wild-type hypophysectomized mice. Finally, urinary excretion of the male-specific, GH pulse-induced major urinary protein was restored to normal male levels following pulsatile GH treatment only in the case of wild-type hypophysectomized mice. STAT5b-deficient mice are thus GH pulse-resistant, supporting the proposed role of STAT5b as a key intracellular mediator of the stimulatory effects of plasma GH pulses on the male pattern of liver gene expression. Growth hormone (GH)1 has diverse effects on metabolism and growth that can result from the direct effects of GH on gene expression, or may be indirectly mediated by factors such as insulin-like growth factor I (1). In addition, the temporal patterns of pituitary GH secretion differ in males and females in many species, resulting in the expression of some genes predominantly in males and other genes predominantly in females (2-4). In male rats, plasma GH pulses are separated by periods of Ͼ2 h during which there is negligible GH detectable in blood. In contrast, the female plasma GH pattern is characterized by a more continuous presence of GH or, in some species such as mice, by more frequent pulses of GH (3,5).GH binds to cell surface receptors that dimerize upon hormone binding and subsequently activate the receptor-associated tyrosine kinase JAK2. JAK2 in turn phosphorylates itself and the GH receptor on multiple tyrosine residues. STAT proteins are then recruited to the GH receptor/JAK2 complex and are phosphorylated on tyrosine and subsequently on serine. STAT proteins activated in this manner form homo-or heterodimers and translocate to the nucleus where they bind to target sites in GH-responsive genes (6, 7). STAT5 proteins in the liver are intermittently, and repeatedly, activated in response to GH pulses (8, 9). GH also activates liver STAT1 and STAT3, but the activation of these STATs is largely ind...

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Proteins in urine scent marks of male house mice extend the longevity of olfactory signals

Cited by 225 publications

References 33 publications

In search of the chemical basis for MHC odourtypes

In search of the chemical basis for MHC odourtypes

Superoxide dismutase deficiency impairs olfactory sexual signaling and alters bioenergetic function in mice

STAT5b-deficient Mice Are Growth Hormone Pulse-resistant

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