Effects of a circadian mutation on seasonality in Syrian hamsters (Mesocricetus auratus)

Loudon, A. S. I.; Ihara, Naomi; Menaker, Michael

doi:10.1098/rspb.1998.0325

Cited by 26 publications

(15 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This corresponds approximately to the time required to experience the same number of melatonin signals as lead to regression in wild type (Fig. 1e) (Loudon et al 1998). Collectively, these data are therefore compatible with the hypothesis that acceleration in the generation of circadian melatonin signal frequency in taus leads to accelerated reproductive and neuroendocrine responses.…”

Section: Seasonal and Photoperiodic Time Measurementsupporting

confidence: 75%

The Biology of the Circadian Ck1εtauMutation in Mice and Syrian Hamsters: A Tale of Two Species

Loudon¹,

Meng²,

Maywood³

et al. 2007

Cold Spring Harbor Symposia on Quantitative Biology

View full text Add to dashboard Cite

INTRODUCTIONThe past decade has witnessed spectacular advances in our understanding of the genetic basis of circadian timing in mammals. The circadian pacemakers within the suprachiasmatic nucleus (SCN) of the hypothalamus provide a crucial function in conducting a circadian repertoire throughout the body, acting on peripheral oscillators in all major body organs and tissues, with profound effects on general systemic physiology (Reppert and Weaver 2002;Hastings et al. 2003;Lowrey and Takahashi 2004;Saper et al. 2005). In both brain and periphery, the molecular clockwork operates as a series of interlocked autoregulatory feedback loops in which CLOCK:BMAL1 heterodimers bind to E-box DNA sequences contained within genes encoding transcriptional repressors PER and CRY. Following their accumulation in the cytoplasm, PER:CRY complexes translocate to the nucleus after a delay of several hours and repress the activity of constitutively bound CLOCK:BMAL1 complexes. These inhibitory complexes are then degraded following a further delay, and the consequent derepression of CLOCK:BMAL1 activity initiates the next circadian cycle of Per and Cry transcription.We have now come to recognize the all-pervasive nature of circadian timing in biology, and the next challenge is to unravel the mechanisms and pathways involved in mediating the effects of the clocks on physiology and metabolism. The general prevalence of many diseases is also marked by a strong circadian component in morbidity, and circadian mutants are often characterized by unexpected side effects in a wide range of pathologies, including malignancy and metabolic and cardiovascular defects. Mutations in various elements of this core molecular clock have been described, many of which result in either arrhythmia or alteration in period of rest/activity and sleep cycles. Genetically mediated desynchronization of central pacemaker function is also strongly implicated as the primary causal mechanism of familial advanced sleep phase syndrome (FASPS), and unraveling the complexities of how circadian mutations act on both central and peripheral pacemakers will reveal important new insight into both the normal regulation of sleep and the pathologies associated with sleep disruption.As in many areas of biology, much of our recent understanding has come from the use of genetically modified mice, allowing studies of incredible sophistication in a species that has an "amenable" genome. Many of the chapters in this volume are devoted to a detailed exposition of the molecular regulation of circadian timing and the impact of clocks on both normal physiology and disease processes. Here, we describe the biology of the first bona fide circadian mutation ever discovered in a mammal, the tau mutation of the Syrian hamster. We explore the impact that this timing mutation has on both the daily and seasonal biology of this species and then describe the same mutation in genetically modified mice. Here, we are able to use the power of mouse genetics to demonstrate some unexpected features of t...

show abstract

Section: Seasonal and Photoperiodic Time Measurementsupporting

confidence: 75%

The Biology of the Circadian Ck1εtauMutation in Mice and Syrian Hamsters: A Tale of Two Species

Loudon¹,

Meng²,

Maywood³

et al. 2007

Cold Spring Harbor Symposia on Quantitative Biology

View full text Add to dashboard Cite

show abstract

“…Data from previous studies on laboratory strains of rodents support the hypothesis that circadian system variation is a source of variation that causes nonresponsiveness to the reproductive effects of SD (Loudon et al, 1998;Puchalski and Lynch, 1986Shimomura et al, 1997;Stirland et al, 1996aStirland et al, , 1996b. In contrast to results from laboratory strains of hamsters, the few previous studies concerning variation in photoresponsiveness in outbred colonies containing natural variation suggest that intraspecific differences in photoresponsiveness between populations are not due to circadian differences.…”

Section: Discussionmentioning

confidence: 56%

“…Similarly, tau mutant Syrian hamsters, which do not respond to SD because the tau mutation accelerates tau from approximately 24 h in the wild type to approximately 20 h in the homozygous mutant (Ralph and Menaker, 1988), will become responsive to SD if the period of the light cycle is manipulated to approximate the mutant free-running period of 20 h (Shimomura et al, 1997;Stirland et al, 1996b). In addition, tau mutants can be made to exhibit gonadal regression under DD (Loudon et al, 1998;Shimomura et al, 1997). Clearly, nonresponsiveness in both Djungarian and tau mutant Syrian hamsters results from a circadian error in measuring photoperiodic time during 24-h cycles seen in natural conditions.…”

Section: Discussionmentioning

confidence: 97%

Tau Differences between Short-Day Responsive and Short-Day Nonresponsive White-Footed Mice (Peromyscus leucopus) Do Not Affect Reproductive Photoresponsiveness

Majoy¹,

Heideman

2000

J Biol Rhythms

View full text Add to dashboard Cite

In laboratory-bred rodent populations, intraspecific variation in circadian system organization is a known cause of individual variation in reproductive photoresponsiveness. The authors sought to determine whether circadian system variation accounted for individual variation in reproductive photoresponsiveness in a single, highly genetically variable population of Peromyscus leucopus recently derived from the wild. Running-wheel activity patterns of male and female mice, aged 70 to 90 days, from artificially selected lines of reproductively photoresponsive (R) and nonresponsive (NR) lines were monitored under short-day photoperiod (8 h light, 16 h dark), long-day photoperiod (16 h light, 8 h dark), and constant darkness (DD). NR mice displayed a significantly longer mean free-running period (24.08 h) in DD compared with R mice (23.75 h), due in large part to a difference between NR and R females (24.25 h vs. 23.74 h, respectively). All other entrainment characteristics (alpha, phase angle of activity) under short days, long days, and DD were similar between R and NR mice. Variation in freerunning period and entrainment characteristics has been shown to affect photoresponsiveness in other rodent species by altering the manner in which the circadian system interprets short days. To determine whether variation in photoresponsiveness in P. leucopus is due to differences in free-running period instead of variation downstream from the central circadian clock in the pathway controlling photoresponsiveness, the authors exposed young R and NR mice to DD and measured the effect on reproductive organ development. If variation in free-running period affected how the circadian system of mice interpreted short days, then both R and NR mice exposed to DD should have exhibited a delay in gonadal development. Only R mice exhibited pubertal delay in DD. NR mice exhibited large paired testes, paired seminal vesicles, paired ovaries, and uterine weight typical of mice nonresponsive to short days, whereas R mice exhibited reproductive organ weight typical of mice responsive to short days. These data suggest that despite significant differences in free-running period between R and NR mice, individual variation in photoresponsiveness is not due to differences in how the circadian systems of R and NR mice interpret the LD cycle.

show abstract

“…Although this has been useful in identifying mechanisms, it has not provided insight into natural variation or led to new insights from that variation. Thus, the hypogonadal mouse (with a genetic defect disabling GnRH production; Mason et al, 1986), tau mutant hamster (with a genetic defect disabling normal circadian rhythms, thus disabling the ability to measure photoperiod normally; Loudon et al, 1998), and fosB knockout mouse (which fails to show normal nurturing behavior toward pups; Brown et al, 1996) have been useful in study of mechanisms, but all mutations of these forms would be highly maladaptive in the wild. In contrast, variation observed in neuroendocrine control of reproductive behavior within and among wild species of mammals is likely to have functional significance and provide insights into normal variation in reproduction and reproductive behavior in other species, including humans.…”

Section: Regulation Of the Seasonal Timing Of Reproductive Behaviormentioning

confidence: 99%

Behavioral neuroendocrinology in nontraditional species of mammals: Things the ‘knockout’ mouse CAN'T tell us

Smale

Heideman

French

2005

Hormones and Behavior

View full text Add to dashboard Cite

The exploration of many of the fundamental features of mammalian behavioral neuroendocrinology has benefited greatly throughout the short history of the discipline from the study of highly inbred, genetically characterized rodents and several other "traditional" exemplars. More recently, the impact of genomic variation in the determination of complex neuroendocrine and behavioral systems has advanced through the use of single and multiple gene knockouts or knockins. In our essay, we argue that the study of nontraditional mammals is an essential approach that complements these methodologies by taking advantage of allelic variation produced by natural selection. Current and future research will continue to exploit these systems to great advantage and will bring new techniques developed in more traditional laboratory animals to bear on problems that can only be addressed with nontraditional species. We highlight our points by discussing advances in our understanding of neuroendocrine and behavioral systems in phenomena of widely differing time scales. These examples include neuroendocrine variation in the regulation of reproduction across seasons in Peromyscus, variation in parental care by biparental male rodents and primates within a single infant rearing attempt, and circadian variation in the regulation of the substrates underlying mating in diurnal vs. nocturnal rodents. Our essay reveals both important divergences in neuroendocrine systems in our nontraditional model species, and important commonalities in these systems.

show abstract

Effects of a circadian mutation on seasonality in Syrian hamsters (Mesocricetus auratus)

Cited by 26 publications

References 22 publications

The Biology of the Circadian Ck1εtauMutation in Mice and Syrian Hamsters: A Tale of Two Species

The Biology of the Circadian Ck1εtauMutation in Mice and Syrian Hamsters: A Tale of Two Species

Tau Differences between Short-Day Responsive and Short-Day Nonresponsive White-Footed Mice (Peromyscus leucopus) Do Not Affect Reproductive Photoresponsiveness

Behavioral neuroendocrinology in nontraditional species of mammals: Things the ‘knockout’ mouse CAN'T tell us

Contact Info

Product

Resources

About