Fluent Essays

you may use the PPTs, notes, and reliable online resources to answer the questions. However, your answers should be in your own words (do not copy and paste directly from the class notes provided). Read each question carefully and include as much detail as possible. Write your answers in full sentences. The powerpoint and the notes from each powerpoints are attached and each each questions has an assign powerpoint slides+notes, so you just need to read the notes and powerpoints to answer the questions. You need to search also to add more data from reliable online sources. you may use the PPTs, notes, and reliable online resources to answer the questions. However, your answers should be in your own words (do not copy and paste directly from the class notes provided). Read each question carefully and include as much detail as possible. Write your answers in full sentences. Q1. Mammalian fetuses develop in conditions dubbed ‘Everest in utero’. Explain what ‘Everest in utero’ refers to and why it is important for normal development. (10pts) Q2. Use the diagram below, which shows human embryonic and fetal development (top of diagram), and major congenital anomalies and function defects in certain organs (blue/green bars). Describe how the normal developmental trajectory is linked to when these anomalies and defects occur and how this is related to the concept of critical windows of development and our ability to understand the effects of teratogens. (12pts) Q3. Describe the following steps in the morphological development of the human heart: (10pts) Formation of heart tube Heart looping Septation Q4. The Fick equation is used to describe embryonic gas exchange. Provide the equation and describe each of its components. Describe how oxygen consumption rate (V̇o2) and oxygen conductance (GO2) increase throughout amphibian development. How do these changes influence PO2 inside the egg? (10pts) Q5. The figure on the left (from Holloway & Geiser 2000 Development of thermoregulation in the sugar glider Petaurus breviceps) shows the difference between body temperature and ambient temperature (Tb-Ta) in sugar gliders of different ages (x axis) at four ambient temperatures (30, 25, 20 and 15°C – each panel). Describe how this figure helps us determine when a sugar glider develops its endothermic ability (maintains a body temperature of ~37°C). (12pts) Q6. What is one tactic used by a bird/reptile embryo in response to thermal variability? Describe an experiment you might perform to investigate this. (12pts) Q7. What are the three main ways by which two environmental stressors may interact with each other? In the figure to the right (from Padilla-Gamino et al 2013 Temperature and CO2 additively regulate physiology, morphology and genomic responses of larval sea urchins, Strongylocentrotus purpuratus) depicting larval sea urchin respiration, describe what two stressors are being examined and the way in which they are interacting to influence larval function. (12pts) Q8. Provide a detailed description of the detrimental effects and mechanism of action of a known endocrine disruptor. (10pts) Q9. Choose one bold option and one underlined option in the sentence below and provide an answer: Provide a summary of why you think phenotypic plasticity/epigenetics/critical windows is/are important for understanding climate change/ocean acidification/human diseases. (12pts) !"#$%##"&' !"#$%&%' (&")*+",'! 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CAU:I5 P( 7&, 4'(#2%&1"% #4 ,-/&* !" #" $%&&%'() (*+ ," -./0.1DAE 40 60 80 100 120 140 160 (a) 40 60 80 100 120 140 160 (b) 40 60 80 100 120 140 160 (d) 40 60 80 100 120 140 160 (c) Age (days) T b –T a( °C ) 25 0 20 15 10 5 25 0 20 15 10 5 25 0 20 15 10 5 25 0 20 15 10 5 ()*+ ,5 ?)&4/%, 7#() &/% #4 ()% 8#<<%*%42% 1%(7%%4 1'83 (%+.%*&(-*% G- 1I &48 &+1#%4( (%+.%*&(-*% G- &I G"-I '< V-0%4#"% !"#$%&%' (&")*+",' &( - &W G&I D; !?R G1I 9: !?W G2I 9; !?R G8I C: !?5 0.5 0.4 0.3 0.2 0.1 0.0 40 60 80 100 120 140 160 Age (days) C on du ct an ce (m l g –1 h –1 ° C –1 ) ()*+ -5 L)%*+&" 2'48-2(&42% &, & <-42(#'4 '< &/% #4 !"#$%&%' (&")*+",' &( &4 &+1#%4( (%+.%*&(-*% G- &I '< 9: !?5 �((%����$#(�#(�'�&*���� � ���$#(�#(����)&#���"�&�����$&������&(��!����� � �������� �&�'$)&���#�"����� � �������� ��%�� �$+#!$������&$"��((%��+++���"�&�����$&���$&�������'(�&��#�*�&'�(,����&�&,��$#������(�������(�� ����� ��')� ��(�($�(�����"�&������$&��(�&"'�$��)'����*��!��!���(��((%��+++���"�&�����$&���$&��(�&"'� 30°C 25°C 20°C 15°C DISCUSSION Petaurusbreviceps,likeallothermarsupials,givesbirth toaltricialyoung.Developmentisslowandittakes about250daysfrombirthtogrowtofullsize.During theearlystagesofpouchlifetheyoungareobviously poikilothermic,andevenbytheageof56dayspossess onlyaverylimitedthermoregulatoryabilitywhichis restrictedtoT a above258C.However,bytheageof95± 100days,andwhentheglidersweighedonly36±42%of adultmass,anincreaseinheatproductionabovethat predictedforadults(Fig.6)andheatretentionmeant thatthegliderswereabletomaintainaconstantT b overaT a rangeofatleast30±158C,althoughata slightlylowerT b thanthatofadults.Furthergrowth wascharacterizedbyasteadydecreaseinmass-speci®c metabolicratetoadultlevels(Fig.6)andaslight increaseinT b ,presumablyresultingfromthedecrease inconductance,untilatadultmassadultlevelswere observed. Thegrowthratesanddevelopmentobservedinthe currentstudyseemtobesimilartothoseofothersugar glidersbornandrearedincaptivity(Smith,1979), suggestingthattheexperimentsconductedheredidnot affectthedevelopmentoftheyoung.Thisisincontrast toHudson(1974),whoobservedreducedgrowthrates inneonatalrodentsBaiomystayloriperiodically removedfromtheirmothersandexposedfor2htoT a 308C.Itisprobablethatremovalofyoungfromtheir mothershasamorepronouncedeffectinrodents,as theygrowfasterthanmarsupials,whichgenerallyhave averyslowrateofdevelopment(Tyndale-Biscoe,1979; Lee&Cockburn,1985).Itwasnoticeableinsugar J.C.HollowayandF.Geiser394406080100120140160 (a) 406080100120140160 (b) 406080100120140160 (d) 406080100120140160 (c) Age (days) T b – T a ( ° C ) 25 0 20 15 10 5 25 0 20 15 10 5 25 0 20 15 10 5 25 0 20 15 10 5 Fig.4.Changeswithageinthedifferencebetweenbodytemperature(T b )andambienttemperature(T a )(DT)ofjuvenile PetaurusbrevicepsatT a :(a)308C;(b)258C:(c)208C;(d)158C. 0.5 0.4 0.3 0.2 0.1 0.0 406080100120140160 Age (days) C o n d u c t a n c e ( m l g – 1 h – 1 ° C – 1 ) Fig.5.ThermalconductanceasafunctionofageinPetaurus brevicepsatanambienttemperature(T a )of258C. 30°C 25°C 20°C 15°C at 138C ( p ! 0.9895, figure 2b). Larvae exposed to 400 matm had higher (35%) respiration rates at 188C than at 138C ( p ! 0.0015), whereas larvae exposed to 1100 matm did not have significantly different respiratory rates between temp- erature treatments ( p ! 0.3122), indicating that elevated pCO2 seems to have counteracted the expected effect of increased temperature on metabolic rate. The decrease in larval metabolic rate at 188C/high pCO2 was reflected in a lower Q10, reduced under high pCO2 from 2.49 to 1.55. There was no significant interaction between temperature and pCO2 (F ! 3.42, d.f. ! 1, p ! 0.079) and no correlation between respiration rate and larval body size ( p ! 0.705). (d) Changes in the transcriptome Genome wide transcriptomics were used to provide mechanis- tic insight into pathways or processes that might be linked to the observations made on two organismal traits—differences in total larval length and respiration rate between experimental conditions. As an initial broad-scale analysis, we used a princi- pal components loading plot to resolve the relationship between temperature, pCO2 and gene expression. This plot revealed that the transcriptomes of larvae raised at 138C were most similar, as the high and low pCO2 treatments at 138C clustered most closely. Transcriptional profiles diverged in larvae raised at 188C as well as between high and low pCO2 treatments (see the electronic supplementary material, figure S3). These expression patterns were corroborated by SVD, which revealed two major patterns of gene expres- sion that collectively accounted for 89 per cent of the total variation in gene expression. The first expression pattern (i.e. eigengene 1, figure 3a) accounted for 64 per cent of the vari- ation and is described by genes whose expression increased in response to elevated temperature and decreased in response to high pCO2 (figure 3a). One-hundred and eleven genes were positively correlated (greater than 0.8) with this expression pat- tern (see figure 3b and electronic supplementary material, table S2a). We used GSEA to identify physiological and cellular processes influenced by the differential expression of these genes. Ontologies relating to the cellular cytoskeleton were by far the most numerous and had the lowest p-values, accounting for 22 of the 42 enriched ontologies (52%) and ontologies with the 11 lowest p-values. Genes driving the enrichment of these cytoskeletal ontologies included multiple isoforms of alpha tubulin and beta tubulin, as well as actin. Other cytoskeletal genes differentially expressed included kinesin-like protein KIF3A (P28741), apextrin (A0T3F5), synte- nin (O00560) and ankyrin domain repeat containing protein 28 (Q9UPS8) (uniprot identifiers in parenthesis; www.uniprot. org). We also surveyed these same 111 genes correlated with eigengene 1 for genes with established roles in larval skeleto- genesis and whose altered expression may be associated with the observed changes in skeletal morphology. Spicule matrix 30 alpha protein (SM30-alpha protein), a major component of urchin larval skeletons [37], was downregulated in larvae raised in high pCO2 water at both temperatures. The pattern responsible for the second largest proportion of variation in expression (i.e. eigengene 2; 25%; figure 3c) described genes decreasing between low and high pCO2 treatments at 188C. Forty-nine genes were positively corre- lated (greater than 0.8) with this expression pattern (see figure 3d and electronic supplementary material, table S2a). As previously explained, we used GSEA to identify larger- scale physiological and cellular processes influenced by the differential expression of these genes. Ontologies relating to nucleosome and chromatin organization and assembly accounted for 14 of 21 significantly over-represented ontolo- gies (67%) and 27 of 49 differentially expressed genes encode histones, structural components of nucleosomes and major regulators of chromatin structure and transcription initiation, processes that are central to the regulation of the cell cycle. Included were histone 2AE, 2AD, 2BF, 2BC, H2B, H3F, H3D, CS-H3, H3 and H3 family 2 isoform 2. Complete GSEA results are shown in the electronic supplementary material, table S2b. Genes encoding skeletal matrix proteins were not present in the set of genes correlated with eigengene 2. 4. Discussion The central goal of this study was to capture the cumulative effects of multiple global change-related stressors on the physiology of calcifying marine larvae. Our integrative approach yielded important findings relevant to the perform- ance of S. purpuratus in future oceans. Firstly, skeletal growth but not developmental rate was influenced by elevated pCO2. Secondly, simultaneous exposure to both increased pCO2 and temperature significantly depressed larval metabolism. Thirdly, transcriptional responses suggest that (i) decreases in skeletal length at high pCO2 may be associated with impaired skeletogenesis, (ii) metabolic depression in response to elevated temperature and pCO2 were associated with reduced expression of multiple histone encoding genes re sp ir at io n ( p m o l O 2 /h r/ la rv a) 0.33(a) (b) 0.32 0.31 0.30 0.29 0.28 0.27 0.26 16 to ta l la rv al l en g th ( m m ) a a b bb a a a 14 12 10 8 6 4 2 0 temperature (°C) 13 18 Figure 2. Physiological performance of S. purpuratus under different temp- erature and pCO2 treatments. (a) Morphometrics and (b) respiration rates. Data are mean + s.e. with different letters indicating statistical significance ( p , 0.05). Skeletal growth differed between pCO2 treatments but did not differ between temperatures. Respiratory rates between pCO2 treatments did not differ at 138C but differed at 188C. Filled bars, 1100 matm; unfilled bars, 400 matm. rspb.royalsocietypublishing.org Proc R Soc B 280:20130155 5 on October 27, 2016http://rspb.royalsocietypublishing.org/Downloaded from Current PCO2 (0.04%) Elevated PCO2 (0.11%) 190 Chapter 5 through adolescence) and thus remains susceptible to insult by environ- mental agents for this extended period. Teratogenic Agents The largest class of human teratogens includes drugs and chemicals (in- cluding heavy metals such as lead and mercury). Although teratogenic effects are usually associated with anthropogenic chemicals (i.e., those produced by humans), some chemicals found naturally in the environment can also cause birth defects. Quinine and alcohol, two common substances derived from plants, also cause developmental abnormalities. Quinine ingested by a pregnant mother can cause deafness, and (as we will de- scribe shortly) alcohol can cause physical and mental abnormalities in her offspring. Viruses, radiation, hyperthermia, and metabolic conditions in the moth- er can also act as teratogens. A partial list of agents that are teratogenic in human embryos and fetuses is provided in Table 5.1. Thalidomide as a teratogenic agent Thalidomide has been difficult to study because it is relatively ineffec- tive in mice and rats, two predominant animals used for developmental toxicity testing. It is also difficult to study because thalidomide becomes metabolized into several products, some of which may be teratogenic and Gilbert Epel 2e Sinauer Associates Morales Studio Gilbert_Epel2e_05.02.ai 02-02-15 Embryonic period (weeks) Fetal period(weeks) Full term 1 2 3 CNS Cleavage, implantation, gastrulation Brain Heart Limbs External genitalia Central nervous system Heart Upper limbs Eyes Lower limbs Teeth Palate External genitalia Ear 4 5 6 7 8 9 16 20–36 38 Functional defects and minor anomalies Major congenital anomalies Common site of teratogen action Disruption results in death HeartEye Eye Teeth PalateEar Ear Figure 5.2 Periods (weeks of gestation) and degrees of sensitivity of embryonic organs to teratogens. The embryonic stage (weeks 3–8) is the period of maximum vulnerability. (After Moore and Persaud 1993.) 05_Gilbert_Epel2E_Chapter05.indd 190 5/21/15 9:46 AM 07/30/2016 - RS0000000000000000000000162184 (Casey Mueller) - Ecological Developmental Biology