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  • 1
    Series available for loan
    Series available for loan
    Distribution of foraminifera in Chaleur Bay, Gulf of St. Lawrence (1978)
    Ottawa : Geological Survey of Canada
    Associated volumes
    Details Availability
    Call number: SR 90.0008(77-30)
    In: Paper
    Type of Medium: Series available for loan
    Pages: 55 S.
    ISBN: 0660015331
    Series Statement: Paper / Geological Survey of Canada 77-30
    Language: English
    Location: Lower compact magazine
    Branch Library: GFZ Library
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  • 2
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    Predicting bird phenology from space: satellite-derived vegetation green-up signal uncovers spatial variation in phenological synchrony between birds and their environment (2015)
    Wiley
    Details
    Publication Date: 2015-10-20
    Description: Population-level studies of how tit species ( Parus spp.) track the changing phenology of their caterpillar food source have provided a model system allowing inference into how populations can adjust to changing climates, but are often limited because they implicitly assume all individuals experience similar environments. Ecologists are increasingly using satellite-derived data to quantify aspects of animals' environments, but so far studies examining phenology have generally done so at large spatial scales. Considering the scale at which individuals experience their environment is likely to be key if we are to understand the ecological and evolutionary processes acting on reproductive phenology within populations. Here, we use time series of satellite images, with a resolution of 240 m, to quantify spatial variation in vegetation green-up for a 385-ha mixed-deciduous woodland. Using data spanning 13 years, we demonstrate that annual population-level measures of the timing of peak abundance of winter moth larvae ( Operophtera brumata ) and the timing of egg laying in great tits ( Parus major ) and blue tits ( Cyanistes caeruleus ) is related to satellite-derived spring vegetation phenology. We go on to show that timing of local vegetation green-up significantly explained individual differences in tit reproductive phenology within the population, and that the degree of synchrony between bird and vegetation phenology showed marked spatial variation across the woodland. Areas of high oak tree ( Quercus robur) and hazel ( Corylus avellana ) density showed the strongest match between remote-sensed vegetation phenology and reproductive phenology in both species. Marked within-population variation in the extent to which phenology of different trophic levels match suggests that more attention should be given to small-scale processes when exploring the causes and consequences of phenological matching. We discuss how use of remotely sensed data to study within-population variation could broaden the scale and scope of studies exploring phenological synchrony between organisms and their environment. Current understanding of how animals synchronise life history events, such as the production of offspring, with the phenology of their food source is limited by the fact that the majority of studies simply correlate average phenotypes across years, neglecting a potentially important spatial dimension in the environment within populations. In this study we use the classic tri-trophic system of passerine songbirds, caterpillars, and deciduous tree to explore whether satellite-derived measures of vegetation spring green-up can be used to predict within-population variation in great tit ( Parus major ) and blue tit ( Cyanistes caeruleus ) breeding phenology. We show that timing of reproduction in both species correlates positively with local vegetation green-up at the population and individual levels, and that there is marked spatial variation across the study site in the strength of this phenological matching, which can be predicted by habitat type.
    Electronic ISSN: 2045-7758
    Topics: Biology
    Published by Wiley
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  • 3
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    The mass-concentration-redshift relation of cold and warm dark matter haloes (2016)
    Oxford University Press
    Details
    Publication Date: 2016-06-01
    Description: We use a suite of cosmological simulations to study the mass–concentration–redshift relation, c ( M, z ), of dark matter haloes. Our simulations include standard -cold dark matter (CDM) models, and additional runs with truncated power spectra, consistent with a thermal warm dark matter (WDM) scenario. We find that the mass profiles of CDM and WDM haloes are self-similar and well approximated by the Einasto profile. The c ( M, z ) relation of CDM haloes is monotonic: concentrations decrease with increasing virial mass at fixed redshift, and decrease with increasing redshift at fixed mass. The mass accretion histories (MAHs) of CDM haloes are also scale-free, and can be used to infer concentrations directly. These results do not apply to WDM haloes: their MAHs are not scale-free because of the characteristic scale imposed by the power spectrum suppression. Further, the WDM c ( M, z ) relation is non-monotonic: concentrations peak at a mass scale dictated by the truncation scale, and decrease at higher and lower masses. We show that the assembly history of a halo can still be used to infer its concentration, provided that the total mass of its progenitors is considered (the ‘collapsed mass history’; CMH), rather than just that of its main ancestor. This exploits the scale-free nature of CMHs to derive a simple scaling that reproduces the mass–concentration–redshift relation of both CDM and WDM haloes over a vast range of halo masses and redshifts. Our model therefore provides a robust account of the mass, redshift, cosmology and power spectrum dependence of dark matter halo concentrations.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press
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  • 4
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    Rare recessive loss-of-function methionyl-tRNA synthetase mutations presenting as a multi-organ phenotype (2013)
    BioMed Central
    Details
    Publication Date: 2013-10-09
    Description: Background: Methionyl-tRNA synthetase (MARS) catalyzes the ligation of methionine to its cognate transfer RNA and therefore plays an essential role in protein biosynthesis. Methods: We used exome sequencing, aminoacylation assays, homology modeling, and immune-isolation of transfected MARS to identify and characterize mutations in the methionyl-tRNA synthetase gene (MARS) in an infant with an unexplained multi-organ phenotype. Results: We identified compound heterozygous mutations (F370L and I523T) in highly conserved regions of MARS. The parents were each heterozygous for one of the mutations. Aminoacylation assays documented that the F370L and I523T MARS mutants had 18 +/- 6% and 16 +/- 6%, respectively, of wild-type activity. Homology modeling of the human MARS sequence with the structure of E. coli MARS showed that the F370L and I523T mutations are in close proximity to each other, with residue I523 located in the methionine binding pocket. We found that the F370L and I523T mutations did not affect the association of MARS with the multisynthetase complex. Conclusion: This infant expands the catalogue of inherited human diseases caused by mutations in aminoacyl-tRNA synthetase genes.
    Electronic ISSN: 1471-2350
    Topics: Biology , Medicine
    Published by BioMed Central
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  • 5
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    Social stress and myelopoiesis [Medical Sciences] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-10-09
    Description: Across a variety of adverse life circumstances, such as social isolation and low socioeconomic status, mammalian immune cells have been found to show a conserved transcriptional response to adversity (CTRA) involving increased expression of proinflammatory genes. The present study examines whether such effects might stem in part from the selective...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not its E3 ligase activity (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-10-29
    Description: Germline mutations of the breast cancer 1 (BRCA1) gene are a major cause of familial breast and ovarian cancer. The BRCA1 protein displays E3 ubiquitin ligase activity, and this enzymatic function is thought to be required for tumor suppression. To test this hypothesis, we generated mice that express an enzymatically defective Brca1. We found that this mutant Brca1 prevents tumor formation to the same degree as does wild-type Brca1 in three different genetically engineered mouse (GEM) models of cancer. In contrast, a mutation that ablates phosphoprotein recognition by the BRCA C terminus (BRCT) domains of BRCA1 elicits tumors in each of the three GEM models. Thus, BRCT phosphoprotein recognition, but not the E3 ligase activity, is required for BRCA1 tumor suppression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904783/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904783/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shakya, Reena -- Reid, Latarsha J -- Reczek, Colleen R -- Cole, Francesca -- Egli, Dieter -- Lin, Chyuan-Sheng -- deRooij, Dirk G -- Hirsch, Steffen -- Ravi, Kandasamy -- Hicks, James B -- Szabolcs, Matthias -- Jasin, Maria -- Baer, Richard -- Ludwig, Thomas -- F31-CA132626/CA/NCI NIH HHS/ -- F32-HD51392/HD/NICHD NIH HHS/ -- P01 CA097403/CA/NCI NIH HHS/ -- P01-CA97403/CA/NCI NIH HHS/ -- R01 CA137023/CA/NCI NIH HHS/ -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-10/HD/NICHD NIH HHS/ -- R01-CA137023/CA/NCI NIH HHS/ -- R01-HD40916/HD/NICHD NIH HHS/ -- T32-CA09503/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2011 Oct 28;334(6055):525-8. doi: 10.1126/science.1209909.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cancer Genetics, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22034435" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/chemistry/*metabolism ; Basic-Leucine Zipper Transcription Factors/genetics/metabolism ; Cells, Cultured ; Disease Models, Animal ; Embryonic Stem Cells/metabolism ; *Genes, BRCA1 ; Ligands ; Mammary Neoplasms, Experimental/*genetics/metabolism ; Mice ; Mutant Proteins/chemistry/genetics/metabolism ; Pancreatic Neoplasms/*genetics/metabolism ; Phosphoproteins/*metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; RING Finger Domains ; Tumor Suppressor Proteins/chemistry/metabolism ; Ubiquitin-Protein Ligases/chemistry/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Transcriptional role of cyclin D1 in development revealed by a genetic-proteomic screen (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-01-22
    Description: Cyclin D1 belongs to the core cell cycle machinery, and it is frequently overexpressed in human cancers. The full repertoire of cyclin D1 functions in normal development and oncogenesis is unclear at present. Here we developed Flag- and haemagglutinin-tagged cyclin D1 knock-in mouse strains that allowed a high-throughput mass spectrometry approach to search for cyclin D1-binding proteins in different mouse organs. In addition to cell cycle partners, we observed several proteins involved in transcription. Genome-wide location analyses (chromatin immunoprecipitation coupled to DNA microarray; ChIP-chip) showed that during mouse development cyclin D1 occupies promoters of abundantly expressed genes. In particular, we found that in developing mouse retinas-an organ that critically requires cyclin D1 function-cyclin D1 binds the upstream regulatory region of the Notch1 gene, where it serves to recruit CREB binding protein (CBP) histone acetyltransferase. Genetic ablation of cyclin D1 resulted in decreased CBP recruitment, decreased histone acetylation of the Notch1 promoter region, and led to decreased levels of the Notch1 transcript and protein in cyclin D1-null (Ccnd1(-/-)) retinas. Transduction of an activated allele of Notch1 into Ccnd1(-/-) retinas increased proliferation of retinal progenitor cells, indicating that upregulation of Notch1 signalling alleviates the phenotype of cyclin D1-deficiency. These studies show that in addition to its well-established cell cycle roles, cyclin D1 has an in vivo transcriptional function in mouse development. Our approach, which we term 'genetic-proteomic', can be used to study the in vivo function of essentially any protein.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943587/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943587/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bienvenu, Frederic -- Jirawatnotai, Siwanon -- Elias, Joshua E -- Meyer, Clifford A -- Mizeracka, Karolina -- Marson, Alexander -- Frampton, Garrett M -- Cole, Megan F -- Odom, Duncan T -- Odajima, Junko -- Geng, Yan -- Zagozdzon, Agnieszka -- Jecrois, Marie -- Young, Richard A -- Liu, X Shirley -- Cepko, Constance L -- Gygi, Steven P -- Sicinski, Piotr -- 15603/Cancer Research UK/United Kingdom -- A15603/Cancer Research UK/United Kingdom -- HG004069/HG/NHGRI NIH HHS/ -- HG3456/HG/NHGRI NIH HHS/ -- P01 CA080111/CA/NCI NIH HHS/ -- P01 CA080111-128270/CA/NCI NIH HHS/ -- P01 CA109901/CA/NCI NIH HHS/ -- P01 CA109901-067138/CA/NCI NIH HHS/ -- P01 CA109901-067140/CA/NCI NIH HHS/ -- R01 CA108420/CA/NCI NIH HHS/ -- R01 CA108420-07/CA/NCI NIH HHS/ -- R01 EY008064/EY/NEI NIH HHS/ -- R01 EY009676/EY/NEI NIH HHS/ -- R01 EY009676-18/EY/NEI NIH HHS/ -- R01 EYO9676/PHS HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-07/HG/NHGRI NIH HHS/ -- R01 HG003456/HG/NHGRI NIH HHS/ -- R01 HG003456-06/HG/NHGRI NIH HHS/ -- R01 HG004069/HG/NHGRI NIH HHS/ -- R01 HG004069-04/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2010 Jan 21;463(7279):374-8. doi: 10.1038/nature08684.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20090754" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; CREB-Binding Protein/metabolism ; Chromatin Immunoprecipitation ; Cyclin D1/deficiency/genetics/*metabolism ; *Gene Expression Regulation, Developmental ; Genome/genetics ; High-Throughput Screening Assays ; Histone Acetyltransferases/metabolism ; Mass Spectrometry ; Mice ; Oligonucleotide Array Sequence Analysis ; Promoter Regions, Genetic/genetics ; Protein Binding ; *Proteomics/methods ; Rats ; Receptor, Notch1/genetics/metabolism ; Retina/cytology/embryology/metabolism ; Stem Cells/cytology/metabolism ; *Transcription, Genetic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 8
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    ATM controls meiotic double-strand-break formation (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-18
    Description: In many organisms, developmentally programmed double-strand breaks (DSBs) formed by the SPO11 transesterase initiate meiotic recombination, which promotes pairing and segregation of homologous chromosomes. Because every chromosome must receive a minimum number of DSBs, attention has focused on factors that support DSB formation. However, improperly repaired DSBs can cause meiotic arrest or mutation; thus, having too many DSBs is probably as deleterious as having too few. Only a small fraction of SPO11 protein ever makes a DSB in yeast or mouse and SPO11 and its accessory factors remain abundant long after most DSB formation ceases, implying the existence of mechanisms that restrain SPO11 activity to limit DSB numbers. Here we report that the number of meiotic DSBs in mouse is controlled by ATM, a kinase activated by DNA damage to trigger checkpoint signalling and promote DSB repair. Levels of SPO11-oligonucleotide complexes, by-products of meiotic DSB formation, are elevated at least tenfold in spermatocytes lacking ATM. Moreover, Atm mutation renders SPO11-oligonucleotide levels sensitive to genetic manipulations that modulate SPO11 protein levels. We propose that ATM restrains SPO11 via a negative feedback loop in which kinase activation by DSBs suppresses further DSB formation. Our findings explain previously puzzling phenotypes of Atm-null mice and provide a molecular basis for the gonadal dysgenesis observed in ataxia telangiectasia, the human syndrome caused by ATM deficiency.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3213282/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3213282/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lange, Julian -- Pan, Jing -- Cole, Francesca -- Thelen, Michael P -- Jasin, Maria -- Keeney, Scott -- F32HD5139/HD/NICHD NIH HHS/ -- GM058673/GM/NIGMS NIH HHS/ -- HD040916/HD/NICHD NIH HHS/ -- HD053855/HD/NICHD NIH HHS/ -- R01 GM058673/GM/NIGMS NIH HHS/ -- R01 GM058673-01/GM/NIGMS NIH HHS/ -- R01 HD040916/HD/NICHD NIH HHS/ -- R01 HD040916-01/HD/NICHD NIH HHS/ -- R01 HD053855/HD/NICHD NIH HHS/ -- R01 HD053855-01A1/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Oct 16;479(7372):237-40. doi: 10.1038/nature10508.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22002603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins/deficiency/genetics/*metabolism ; Chromosome Segregation ; *DNA Breaks, Double-Stranded ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Endodeoxyribonucleases/biosynthesis/genetics/metabolism ; Feedback, Physiological ; Gene Dosage ; Male ; *Meiosis ; Mice ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Spermatocytes/metabolism ; Testis/cytology/metabolism ; Tumor Suppressor Proteins/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    Liability Structure in Small-Scale Finance: Evidence from a Natural Experiment (2013)
    Oxford University Press
    Details
    Publication Date: 2013-11-22
    Description: Microfinance, the provision of small individual and business loans, has experienced dramatic growth, reaching over 150 million borrowers worldwide. Much of the success of microfinance has been attributed to attempts to overcome the challenges of information asymmetries in uncollateralized lending. However, very little is known about the optimal contract structure of these loans, and there is substantial variation across lenders, even within a particular setting. This paper exploits a plausibly exogenous change in the liability structure offered by a microfinance program in India, which shifted from individual to group liability lending. We find evidence that the lending model matters: for the same borrower, the required monthly loan installments are 11 percent less likely to be missed under the group liability setting in comparison with individual liability. In addition, compulsory savings deposits are 20 percent less likely to be missed under group liability contracts.
    Print ISSN: 0258-6770
    Electronic ISSN: 1564-698X
    Topics: Economics
    Published by Oxford University Press
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  • 10
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    Incubation behavior adjustments, driven by ambient temperature variation, improve synchrony between hatch dates and caterpillar peak in a wild bird population (2017)
    Wiley
    Details
    Publication Date: 2017-10-12
    Description: For organisms living in seasonal environments, synchronizing the peak energetic demands of reproduction with peak food availability is a key challenge. Understanding the extent to which animals can adjust behavior to optimize reproductive timing, and the cues they use to do this, is essential for predicting how they will respond to future climate change. In birds, the timing of peak energetic demand is largely determined by the timing of clutch initiation; however, considerable alterations can still occur once egg laying has begun. Here, we use a wild population of great tits ( Parus major ) to quantify individual variation in different aspects of incubation behavior (onset, duration, and daily intensity) and conduct a comprehensive assessment of the causes and consequences of this variation. Using a 54-year dataset, we demonstrate that timing of hatching relative to peak prey abundance (synchrony) is a better predictor of reproductive success than clutch initiation or clutch completion timing, suggesting adjustments to reproductive timing via incubation are adaptive in this species. Using detailed in-nest temperature recordings, we found that postlaying, birds improved their synchrony with the food peak primarily by varying the onset of incubation, with duration changes playing a lesser role. We then used a sliding time window approach to explore which spring temperature cues best predict variance in each aspect of incubation behavior. Variation in the onset of incubation correlated with mean temperatures just prior to laying; however, incubation duration could not be explained by any of our temperature variables. Daily incubation intensity varied in response to daily maximum temperatures throughout incubation, suggesting female great tits respond to temperature cues even in late stages of incubation. Our results suggest that multiple aspects of the breeding cycle influence the final timing of peak energetic demand. Such adjustments could compensate, in part, for poor initial timing, which has significant fitness impacts. In this study, we examined whether incubation behavior is used to improve hatching synchrony, and which temperature cues best predict within-year variation in incubation. We found that hatching synchrony is significantly altered by both the onset and duration of incubation behavior, with resulting impacts on reproductive success. We also showed that females are responding to temperatures right through incubation, altering daily intensity based on daily maximum temperatures.
    Electronic ISSN: 2045-7758
    Topics: Biology
    Published by Wiley
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