Environmental Physiology of Livestock (Collier/Environmental Physiology of Livestock) || Regulation of Acclimation to Environmental Stress

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P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mmChapter 4Regulation of Acclimation toEnvironmental StressKajal Sankar Roy and Robert J. CollierWhat Is Acclimation?A variety of environmental factors such as ambient temperature, solar radiation, relativehumidity, and wind speed are known to have direct and indirect effects on domestic animals(Collier et al., 1982, 2004, 2005). The direct effects involve impacts of the environment onthermoregulation, the endocrine system, metabolism, production, and reproduction. Indirecteffects include impacts of the environment on food and water availability, pest and pathogenpopulations, and resistance of the immune system to immunologic challenges. Animals havedeveloped copingmechanisms tominimize the impact of these environmental stressors on theirbiological systems. These responses are broadly described as acclimation, acclimatization, andadaptation. Acclimation is the coordinated phenotypic response developed by the animalto a specic stressor in the environment (Fregley, 1996), while acclimatization refers tothe coordinated response to several individual stressors simultaneously (e.g., temperature,humidity, and photoperiod; Bligh, 1976). In general, there is hardly ever a case in the naturalenvironment where only one environmental variable changes. Thus, in the vast majority ofcases the animal is undergoing acclimatization to the changing environment. Acclimation andacclimatization involve phenotypic and not genotypic change, and the acclimation responseswill decay if the stress is removed. The overall impact of acclimation and acclimatization is toimprove the tness of the animal in the environment. In many cases the acclimation response isinduced by sudden environmental change. In other examples the acclimation response is drivenby changes in photoperiod or other environmental cues such as the lunar cycle, which permit theanimal to anticipate the coming change in the environment leading to seasonal acclimationadjustments in insulation (coat thickness, fat deposition), feed intake, or reproductive activityin advance of the actual environmental change. However, in every case, the process is drivenby the endocrine system and is homeorhetic. Homeorhesis is dened as the coordination ofEnvironmental Physiology of Livestock, First Edition. Edited by R. J. Collier and J. L Collier.C 2012 John Wiley & Sons, Inc. Published 2012 by John Wiley & Sons, Inc.49P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mm50 Environmental Physiology of Livestockmetabolism to support a specic physiologic state (Bauman and Currie, 1984). In this casethe specic physiologic state is the acclimatized animal.Adaptation: Bos indicus versus Bos taurusIf environmental stressors are present for prolonged periods of time (e.g., years) the metabolicand physiologic adjustment can become xed genetically and we refer to this state as theadapted state of animal. Examples are Bos indicus breeds of cattle, which have evolved underconditions of high temperature and humidity and display a number of genetic differences thatendow them with improved thermotolerance, compared to Bos taurus breeds of cattle, whichevolved under temperate weather conditions.Bos indicus cattle have greater thermoregulatory capability than Bos taurus. As pointedout by Hansen (2004), Bos indicus cattle produce less heat, have increased capacity to loseheat toward the environment, or a combination of both. This suggests that low metabolic ratesresulting from reduced growth rates and milk yields of many Indicus breeds constitute a majorcontributing factor to thermotolerance. The basal metabolic rate of B. indicus is in fact lowerthan that for B. taurus (Finch, 1985). The physiological and cellular basis for this differencehas not been identied. One possibility for improved heat loss in B. indicus is that the density ofarteriovenous anastomoses is higher in B. indicus. Since these structures have lower resistanceto ow than vascular passages involving capillary networks, they facilitate increased bloodow to the skin during heat stress (Hales et al., 1978).The vascularity and degree of insulation of the skin and quality of the hair coat (hair andskin coat color, thickness and density of hair bers) also contribute to the effectiveness ofheat loss in cattle (Gebremedhin et al., 2008, 2010). All of these are affected by breed andcontribute to well-known genotype environment effects.The actual rate of heat loss via sweating depends not only upon the extrusion of water at theskin surface but also upon the evaporation of that water. It has been observed that evaporativeheat loss rates were less affected by humidity for Indicus cows than for Holstein and BrownSwiss cows. For example, studies showed that the sweating rate in Indicus cattle exposedto heat stress was unaffected by humidity of the surrounding air while the sweating rate ofShorthorn cattle was reduced as humidity increased (Finch, 1985). This result was interpretedas reecting the greater trapping of humidied air in the dense hair coat of the Shorthorns.There is no evidence that respiratory capacity for heat loss is superior for Indicus cattle. Theproportion of evaporative heat lost via respiration was roughly similar for Indicus, Holstein,Jersey, and Brown Swiss (Kibler and Brody, 1952). During heat stress, evaporative heat loss viarespiration rate can be greater for European breeds and this occurrence also probably reectsthe greater engagement of heat loss mechanisms for the less-adapted breeds.There is a general belief that the appendages of B. indicus cattle contribute to their superiorthermoregulatory ability, as the appendages increase the surface area per unit body weight ascompared to B. taurus. The actual importance of these anatomical features is not likely to becrucial for thermoregulation because surgical removal of the dewlap or hump of Red Sindhibulls did not have a measurable impact on thermoregulatory ability (McDowell et al., 1958).Additionally, differences in regulation of rectal temperature in response to heat stress wereobserved between Jersey and Red Sindhi Jersey even though surface area per unit bodyweight or metabolic body weight was similar between the two genotypes.Heat stress has less severe effects on semen quality of Indicus bulls than it does on bulls ofEuropean breeds, and this phenomenon reects not only adaptations that affect whole-bodyP1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mmRegulation of Acclimation to Environmental Stress 51thermoregulation but also specic adaptations that enhance the local cooling of blood enteringthe testis. A study by Brito et al. (2004) demonstrated that the anatomical features of thetesticular thermoregulatory systemdiffered betweenNelore, crossbred (5/8 or 5/16CharolaisZebu) and Angus bulls. For example, the ratio of testicular artery length to testicular volumewas greatest for Nelore bulls, intermediate for crossbred bulls, and least for Angus bulls. Inaddition, the testicular artery wall thickness and the distance between arterialvenous bloodin the testicular vascular cone were least in Nelore, intermediate in crossbreds, and greatestin Angus. These anatomical differences were related to differences in testicular intra-arterialtemperature, which was lowest in Nelore, intermediate in crossbreds, and highest in Angus(Brito et al., 2004).When animals are adapted the physiologic differences between them and non-adaptedanimals do not disappear when the environment changes. This is not the case in acclimationwhere differences do disappear if the stress is removed. However, it is becoming clear that thesame systems that are involved in acclimatization are the systems that endow animals withthermotolerance or adaptation to heat. Therefore, obtaining a better understanding of the genenetworks involved in response to environmental stress will also lead us to those pathwayswhich offer promise to improve thermotolerance.Acclimatization requires several days to weeks to fully develop, there is a hormonal linkbetween the central nervous system and the effector cell types involved, and the effect ofthe hormonal change is to alter the responsiveness of the effector cells to environmentalchange (Bligh, 1976). These key features are hallmarks of a homeorhetic process in whichmetabolism of multiple tissues and organs is coordinated to support the new acclimatizedstate as contrasted to a homeostatic process (Bauman and Currie, 1984; Collier et al., 2004),and where regulation is occurring around a set point. We then need to consider the stages ofacclimation, the hormones that are driving acclimation, and what changes are occurring ineffector tissues to accomplish development of the acclimatized state.What Are the Stages of Acclimation?Acclimatization is generally considered to occur in two stages: acute or short term and chronicor long term (Johnson and Vanjonack, 1976; Horowitz, 2002; Garrett et al., 2009). Theacute phase includes a shock response at the cellular level (Carper et al., 1987; Sonna,2002) and homeostatic endocrine, physiological, and metabolic responses at the systemiclevel. The chronic or long-term phase results in acclimation to the stressor and involves thereprogramming of gene expression and metabolism (Horowitz, 2002; Collier et al., 2006).In agricultural animals there is generally a loss in productivity as animals progress throughthe acute phase and some or even all of this productivity is restored as animals undergoacclimation to the stress.What Is Involved in the Systemic Response?The systemic response to environmental stress is driven by two systems: (1) the central nervoussystem (CNS) and (2) peripheral nervous system and endocrine components (Charmandariet al., 2005). The central component is comprised of nuclei in the hypothalamus and thebrainstem, which release corticotropin-releasing hormone (CRH) and arginine vasopressin(AVP). The peripheral components of the stress system include the pituitary-adrenal axis,P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mm52 Environmental Physiology of Livestockthe efferent sympathetic-adrenomedullary system, and components of the parasympatheticsystem (Habib et al., 2001). However, relative to environmental stress and acclimation, theinitial phases of the response involve receptor systems at the periphery that drive autonomicand endocrine responses to the changing environment (e.g., skin thermoreceptors andphotoreceptors in the retina).Sweating and panting are two of the primary autonomic responses exhibited by animalsunder heat stress. Sweating results in increased evaporative heat loss from the skin surface,whereas in panting, sensible heat from the body core is used to heat the water vapor and expelheat in the form of vaporized moisture from the lungs. However, these responses are likelydriven more by surface temperatures than core body temperatures. As shown in Figures 4.1and 4.2, evaporative heat loss from skin and the respiratory tract is highly correlated with skintemperature. In fact, skin temperature is more highly correlated with these parameters thancore temperature suggesting that thermal receptors in the skin initiate the autonomic systemicresponse to thermal stress. Another potential route of information ow from the surface to thewhole system would be via secreted heat shock protein (HSP) released from skin epitheliumduring heat stress, whichwould act as an alarm system to assist inmobilizing the acute responseto thermal shock. An examination of the relationship between skin temperature and expressionof the gene for inducible heat shock protein 70 (see Fig. 4.3) revealed that gene expression isincreased several-fold as skin temperature approaches 35C, which is below body temperaturebut represents the upper limit of the thermoneutral zone of cattle. Berman (2005) estimated thatthe stress response system in cattle would be activated at effective temperatures at and above35C. Previously, it has been demonstrated that evaporative heat loss and rectal temperaturerise dramatically above an effective environmental temperature of 35C (see gs. 4.1 and 4.2;Collier et al., 2008). It is now apparent that the heat shock response in bovine skin epithelialtissue is activated at effective environmental temperature of 35C as well. Activation of theheat shock response in cells in many cases leads to secretions of HSPs into the extracellularspace and plasma (Ireland et al., 2007). 35.0 40.0Breaths per Minuter = 0.73, P < 0.0001Surface Temperature (C)Figure 4.1. Correlation of left side surface temperature and respiration rate in Holstein cows in asemi-arid environment.P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mmRegulation of Acclimation to Environmental Stress 53y = 1.1665x2 64.166x + 894.35R2 = 0.4348y = 4.2976x 71.289R2 = 0.0368 < 35C > 35C05020 25 30 35 40 45 50100150200250300350Surface Temperature (C)Sweating rate (g/m2 per h)Figure 4.2. Relationship between infrared coat surface temperature and evaporative heat loss (EVHL)in Holstein dairy cows. Open circles and regression correlation (R2 = 0.4348) denote EVHL below35C. Closed circles and regression correlation (R2 = 0.0358) denote EVHL above 35C. Slopes of tworegressions differ, P < 0.001.Figure 4.3. Relationship between skin temperature and fold increases in heat shock protein 70 geneexpression in cattle skin.P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mm54 Environmental Physiology of LivestockRecently, secreted heat shock protein was identied in plasma of cattle. Kristenson andcolleagues (2004) in Australia have demonstrated that secreted HSP concentrations rise inplasma when the effective environmental temperature exceeds 35C (Gaughan and Bonner,2009). Thus, activation of the heat shock response in cells also leads to secretion of HSPs intothe extracellular space and plasma (Ireland et al., 2007). It has been hypothesized that secretedheat shock protein acts as an alarm signal for the immune system and several measures ofinnate immunity are increased following increases in secreted heat shock protein in blood(Fleshner and Johnson, 2005). Secreted heat shock protein has also been shown to improvesurvival of neural cells subjected to environmental and metabolic stressors (Tytell, 2005;Guzhova et al., 2001).Thus, the acute response in cattle is initially driven by thermal receptors in skin thatactivate the CNS and subsequently, the endocrine system and the peripheral components of theautonomic system. This response is augmented by secreted HSPs that rapidly rise in plasmaand are believed to provide protective effects to a variety of cell types as well as activatingthe innate immune system. At a skin surface temperature of 35C the respiration rate of cattlewill reach or exceed half maximal which is about 60 to 70 breaths per minute (see Fig. 4.1).At this point, the animal is entering the acute phase of the stress response.During the acute phase there is rapid decline in productivity of domestic animals and thisis especially true in high producing dairy cows. The decline in productivity begins on the daythe stress is initiated but is not maximal until 48 hours following the initiation of the stress(Collier et al., 1981). This suggests there are intermediate events between the rise in bodytemperature and the reduction in milk yield. Rhoads et al. (2009) demonstrated that reducedfeed intake only accounted for 40% of the decline in milk yield and that other factors werelikely involved in the rapid decline in production to severe heat stress. They postulated thatreduced glucose availability could potentially reduce lactose synthesis rates and contribute tothe reduced milk volume. Silanikove et al. (2009) reported that acute heat stress reduced milksecretion in lactating cows by up-regulating the activity of a milk-borne negative feedbackregulatory system, specically an n-terminal fragment of -casein. They also reported thatthis fragment has an inhibitory activity on the mammary epithelial cell potassium channel.Identication of the exact mechanisms by which milk yield is reduced in response to heatstress offers potential in improving productivity of animals in warm climates.After ve to seven days of continuous stress, animals enter the chronic acclimation phaseof the stress response. During this phase there is a reprogramming of metabolism resulting inaltered responses to homeostatic signals. The overall impact of these changes is a reduction inthe impact of the stress on the animal. The transition of animals from the acute to the chronicphase of the stress response has been extensively studied in laboratory models by Horowitzand coworkers (Horowitz, 2002; Horowitz et al., 2004; Maloyan et al., 2005; Horowitz, 2007).These changes are driven by the endocrine system and result in global changes in geneexpression as well as post-translational alterations in protein function. Hormones that havebeen identied as being homeorhetic regulators are also linked to acclimation responsesto thermal stress and changes in photoperiod related to season. These hormones includesomatotropin, prolactin, thyroid hormones, glucocorticoids, and mineralocorticoids. Severalof these hormones are known to contribute to regulation of HSP gene expression, as noted inTable 4.1. The changes that occur at the cellular level and provide improved cytoprotection aredescribed in the section on the cellular response to heat stress.At the systemic level, metabolism is coordinated to support a new physiological state. Someof the changes that occur include a lowering of the threshold for vasodilation and evaporativeP1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mmRegulation of Acclimation to Environmental Stress 55Table 4.1. Partial list of hormones affecting heat shock protein (HSP) gene expression or protein activityHormone Effect ReferenceACTH Stimulates HSP production Blake et al. 1991,1994Insulin Stimulates HSP gene in cardiac tissue Li et al. 2006IGF-1 Increased HSPs in epidermis of IGFtransgenic miceShen et al. 2007Prolactin Stimulates HSP-60 in rodent luteal cells Stocco et al. 2001Growth Hormone Stimulates HSP in whole blood of SeaBreamDeane & Woo 2005Glucocorticoids Increases cytosol HSPs and HSP geneexpressionVijayan et al. 2003Melatonin Increases HSP gene expression inpancreatic AR42J cellsBonior et al. 2005Leptin Down regulates HSP-70 in chicken liverand hypothalamusFigueiredo et al. 2006Vasopressin Stimulates HSP in renal tubular cells Xu et al. 1996Catecholamines Stimulates HSP in Brown Adipose tissue Matz et al. 1996Prostaglandin A Increased expression of HSP in bovine Collier et al. 2007Mammary epithelial cells & human K562 Amici et al. 1992Cells and human monocytes Elia et al. 1999Estrogensa & Androgens Increased HSP gene expression in humanneuronsZhang et al. 2004Adapted from Collier et al. (2008).cooling (Roberts et al., 1977), reduced metabolic rate, increased resistance to thermal injury,and improved cardiac performance (Horowitz, 2002). Endocrine changes occurring with ac-climation to heat stress in cattle include increased plasma prolactin, reduced glucocorticoid,somatotropin, and thyroxine concentrations, and in pregnant cattle endocrine changes led toincreased progesterone concentrations and decreased estrone sulfate concentrations (Collieret al., 2004). Somatotropin is a homeorhetic regulator and has been shown to be benecialin improving evaporative heat loss and thermal balance in cattle during summer heat stress(Manalu et al., 1991). Despite large reductions in feed intake and energy balance during heatstress there appears to be a tighter coupling of the somatotropin-IGF axis during summer,resulting in higher IGF concentrations during summer months compared to winter months andonly slight decreases in plasma IGF to severe heat stress even when somatotropin concentra-tions are reduced (Collier et al., 2008; Rhoads et al., 2009). This fact reinforces the importanceof somatotropin in dealing with environmental stress (Collier et al., 2005). Additionally, thesomatotropin response to GRF is not affected by severe heat stress (Rhoads et al., 2009). Theseasonal variation in coupling of the growth hormone-IGF axis is also associated with effectsof increased photoperiod on growth rate and milk yield in cattle (Collier et al., 2006).Cellular Heat Shock ResponsesHeat tolerance at the cellular level is directly related to the ability of the cell to maintainelevated levels of heat shock proteins (HSPs). As stated by Horowitz and Assadi (2010), Ahallmark of the acclimation process is the enhancement of cytoprotective networks that ofthe heat shock proteins, anti-oxidative and apoptotic and the stabilization of the HypoxiaInducible Factor (I), the master regulator of oxygen homeostasis.P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mm56 Environmental Physiology of Livestockad e fb cFigure 4.4. Regression of ductal structures in response to 24 hours of heat stress; samples representthree separate cultures in which control samples (a, b, c) were cultured at 37C but were otherwise treatedidentical to the thermal stress (42C) samples (d, e, f).The heat shock response of bovine embryos and mammary epithelial cells to heat stress hasbeen described (Edwards et al., 1997; Jousan and Hansen, 2004; Collier et al., 2006, 2008).The dramatic effect of heat shock on mammary epithelial cell growth and structure is shownin Figure 4.4. Heat shock acutely down-regulates DNA synthesis and adversely affects theability of cells to maintain their cytoskeleton, leading to a collapse of cell structure.The transcriptome prole of heat-shocked bovine mammary epithelial cells indicated down-regulation of genes involved in cell structure, DNA synthesis, cell division, metabolism,biosynthesis, and intracellular transport, while genes associated with cellular and proteinrepair and degradation were up-regulated. The up-regulation of the heat shock family ofproteins during thermal stress is characterized in Figure 4.5 which displays the pattern ofHSP-70 gene expression during thermal shock. Also apparent in Figure 4.5 is the drop inexpression of HSP-70 message after four hours at 42C. At the cellular level, loss of HSPexpression coincides with loss of thermotolerance and initiation of apoptosis. The heat shockresponse is induced by accumulation of misfolded proteins in the cytoplasm and is mediatedby heat shock transcription factors (HSF; Voellmy and Boellmann, 2007). There are fourforms of HSF but HSF-1 is considered to be the primary transcription factor involved in theheat shock response (Akerfelt et al., 2007). Regulation of HSF-1 activity has been reportedto be largely controlled post-translationally and not at the level of synthesis/degradation ofthe transcription factor (Voellmy and Boellmann, 2007). Once activated, the HSF-1 monomertrimerizes with other HSF-1 molecules, which is essential for DNA binding (Sarge et al.,P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mmRegulation of Acclimation to Environmental Stress 5705101520250 1 2 4 8 16 24Expression (2^ddCT) Time from HS Effect of Thermal Shock on HSP-70 Expression Figure 4.5. Effect of thermal stress (42C) on Heat Shock Protein 70 gene expression in culturedbovine mammary epithelial cells.1993). The activated complex can then enter the nucleus and initiate transcription of heatshock proteins.Thermal acclimation and thermal adaptation are associated with increased basal levels ofHSPs (Carpar et al., 1987; Kregel, 1992; Maloyan et al., 1999). Thermal acclimation andcyclopentenone prostaglandins have been shown to increase the DNA-binding activity ofHSF-1 leading to increased HSP gene transcription (Amici et al., 1992; Straus and Glass,2001; Ianaro et al., 2003; Buckley and Hofmann, 2002). Several investigators have shown thatheat acclimation also provides cross-tolerance against other types of stress such as hypoxia,ischemia, acidosis, and energy depletion (Horowitz, 2002; Kregel et al., 2002), and that HSF-1is involved in this process. Although there is little evidence for endocrine regulation of HSF-1gene expression activity there is substantial evidence that expression of heat shock proteinsand other cytoprotective proteins are modulated by the endocrine system. A partial list ofhormones affecting heat shock protein gene expression is shown in Table 4.1.The separate evolution of Bos taurus, Bos indicus, and Sanga cattle has resulted in differinggenotypes of Bos indicus and Sanga cattle that confer improved thermotolerance comparedto Bos taurus cattle in both beef and dairy populations (Paula-Lopes et al., 2003; Hansen,2004). In addition, large genotype environment interactions in dairy cattle for milk yield(Ceron-Munoz et al., 2004; Ravagnolo et al., 2000; Bohmanova et al., 2006) for Holsteincattle indicate that there is considerable opportunity to improve thermal resistance and per-formance in dairy cattle. These differences include thermoregulatory capability, feed intakeand production responses, and cellular differences in heat shock responses (Hansen, 2004;Collier et al., 2008).There are genetic differences in cellular resistance to elevated temperature in cattle. Itis possible that the same gene or genes conferring cellular thermotolerance are present inIndicus, Senepol, and Romosinuano, especially because of the contribution of B. indicusgenotypes to these two other breeds (Magee et al., 2002). An alternative explanation is thatP1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mm58 Environmental Physiology of Livestockdistinct thermotolerance genes are present in the different genotypes. Identication of thegenes conferring cellular thermotolerance offers the possibility of transferring these genes toheat-sensitive breeds to improve reproduction and other physiological systems compromised byhyperthermia. Little is known regarding themolecular basis for the improved cellular resistanceto elevated temperature in thermotolerant cattle. There were no detectable differences betweenIndicus, Senepol, and Angus in the amount of heat shock protein 70 (HSP-70) in heat-shockedlymphocytes (Kamwanja et al., 1994) although the tendency for lower cellular concentrationof HSPs in Brahman and Senepol may indicate that protein denaturation in response toelevated temperature (one of the signals for HSP-70 synthesis; Shamovsky and Nudler, 2008).The capacity for transcription in response to elevated temperature seems to be importantfor expression of genetic differences because there were no differences between Indicus andHolstein embryos in resistance to elevated temperature at the two-cell stage, a time whenthe embryonic genome is largely inactive (Hansen, 2004). Also, in vitro effects of elevatedtemperature on spermatozoa were similar for Indicus, Indicus-inuenced breeds, Angus, andHolstein (Block et al., 2002).The cellular thermotolerance of crossbred embryos is dependent upon the genotype of theoocyte and not the spermatozoa. Embryos produced by insemination of Brahman oocytes withAngus spermatozoa were more thermotolerant than embryos produced by insemination ofHolstein oocytes with Angus semen (Block et al., 2002). In contrast, there were no differencesin thermotolerance between Indicus Holstein embryos and Angus Holstein embryos.These results indicate that either genes conferring thermotolerance are paternally imprinted(only the maternal allele is expressed) or thermotolerance in embryos depends upon somegenetically controlled factor produced in the oocyte. Regulation of body temperature is themost critical factor for genetic differences in reproductive function during heat stress sincethe depression in fertility per unit increase in body temperature is the same for B. indicus B. taurus crossbred cows as for Hereford Shorthorn cows (Hansen, 2004).New genomics tools are also beginning to provide information on specic gene networksassociated with thermotolerance. Lillehammer et al. (2009) identied single nucleotide poly-morphisms (SNPs) that were associated with gene environment interactions for productiontraits in cattle. Hayes et al. (2009) also reported on a genome-wide association study aimedat identifying differences related to adaptation to environmental change. It is envisioned thatin the not too distant future use of SNP markers will lead to greater progress in improvingthermotolerance of high producing dairy breeds.ConclusionAcclimation is a homeorhetic process driven by the endocrine system, which enables animalsto respond to a stress. The resulting cellular, metabolic and systemic changes associated withacclimation reduce the impact of the stress on the animal and allow it to function moreeffectively in the stressful environment. These changes are lost if the stress is removed sothe process is not based on changes in the genome. However, if the stressful environment isnot removed over successive generations these changes will become genetically xed andare referred to as adaptations. A better understanding of genetic differences between adaptedanimals will contribute useful information on the genes associated with acclimation. Likewise,study of gene expression changes during acclimation will assist in identifying genes associatedwith improved thermotolerance.P1: SFK/UKS P2: SFKBLBS093-c04 Collier October 29, 2011 10:11 Trim: 244mm172mmRegulation of Acclimation to Environmental Stress 59ReferencesAkerfelt, M, D Trouillet, V Mezger, and L Sistonen. 2007. Heat shock factors at a crossroadbetween stress and development. Ann NY Acad Sci. 1113:1527.Amici, C, L Sistonene, M Gabriella Santoro, and RI Morimoto. 1992. Antiproliferativeprostaglandins activate heat shock transcription factor. Proc Natl Acad Sci. 89:62276231.Bauman, DE, and WB Currie, 1980. Partitioning of nutrients during pregnancy and lac-tation: A review of mechanisms involving homeostasis and homeorhesis. J Dairy Sci.63(9):15141529.Berman, A. 2005. Estimates of heat stress relief needs for Holstein dairy cows. J Anim Sci.13771384.Blake, MJ, R Udelsman, GJ Feulner, DD Norton, and NJ Holbrook. 1991. 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