Integrating Concepts in Biology PowerPoint Slides for Chapter 23: Homeostasis at the Organismal Level Section 23.1 by A. Malcolm Campbell, Laurie J. Heyer, and Chris Paradise Title Page

Homeostasis of Morphology Opening Art: UN Figure Homeostasis at the organismal level can result in divergent outcomes from a sumo wrestler in Japan to a world-class distance runner in Kenya. Opening Figure

Body Temperature Homeostasis Figure 23.1 Body temperature vs. ambient temperature of mammals and reptiles. (a) Body temperature as it varies with ambient temperature for eight animals. Mammals are represented with circles, reptiles as triangles. (b) Effect of environmental temperature on human internal body and skin temperatures. Error bars represent standard deviations. Fig. 23.1

Season Dimorphism in Arctic Fox Figure 23.2 Seasonal dimorphism in the arctic fox. Summer (a) and winter (b) coats of the arctic fox (Alopex lagopus). Fig. 23.2

Fur Adjusts to Seasonal Weather change (% of August) Figure 23.3 Changes in arctic fox fur and body temperatures. (a) Percent change in hair length on different part of the body in January compared to August. Significant differences are purple. (b) Overall average monthly fur length (open circles) and body minus ambient temperature (red circles), both expressed as a percentage of August means. The bar at the bottom shows the relative amounts of daily sunlight as it decreases, increases, or is constant. Fig. 23.3

Season Dimorphism in Camels Figure 23.4 Seasonal dimorphism of camel fur. (a) Winter and (b) summer coats of the camel Camelus dromedarius. These individual animals live in temperate zoological parks in Europe. Fig. 23.4

Core Body Temperature Variations Figure 23.5 Body temperature of camels. Two representative rectal temperature records of camels. Noon is represented by the numbers on the x-axis, and midnight by the hash marks. Fig. 23.5

Loss of Cat Temperature Regulation Figure 23.6 Thermoregulation of cat after surgical manipulation of hypothalamus. The eleven lines represent the core body temperatures for experimental cats when maintained in a room of the indicated temperature. The cat’s temperature was subtracted from the average of 101.4 before graphing. Each colored line represents a different cat and the length of the line indicates how long the cat lived. Fig. 23.6

Temperature Responsive Neurons Figure 23.7 Cat thermoregulation responds to manipulation of hypothalamus. (a) Measurements from a single hypothalamus neuron which was gently heated in an anesthetized cat, and its rate of action potentials was quantified. (b) Correlation between the cat’s hypothalamus neuronal activity and the animals breathing rate. Fig. 23.7

Horse Anatomy Helps Thermoregulation Figure 23.8 Thermoregulation in exercising horses. (a) Anatomy of horse head with hypothalamus and cavernous sinus labeled. (b) Experimental set up with horse on treadmill. (c) Temperatures as horse increases speed from 1 to 7 meters per second (m/s) until it stopped, as indicated. (d) Similar data but the horse had its airway surgically diverted away from sinuses. Fig. 23.8

Human Thermostat Maintains 37° C Figure 23.9 Human thermoregulation with experimental manipulation. In a series of independent experiments, one man had his skin chilled to the indicated temperatures while investigators monitored his metabolic heat production (black symbols and lines) or heat loss in the form of evaporated sweat (open triangles and blue line). Cranial temperature was determined by measuring the eardrum. Fig. 23.9

2009 Paper Gender Distribution Figure ELSI 23.1 Gender information from articles published in 2009. Investigators quantified the frequency the study organisms of biological research papers were male, female, both or uncertain. Fig. ELSI 23.1

Obesity Epidemic in America Figure 23.10 Obesity is an epidemic in America. (a) Percent American children classified as obese. (b) Percentage of obese teens analyzed by gender and ethnicity. (c) Percentage of high school students who get one or more hours of exercise per week, analyzed by gender and ethnicity. Fig. 23.10

Physiology of Body Fat Homeostasis Figure 23.11 Rat brain helps regulate body mass. (a) Dissected rat brain viewed from below (ventral side) at the conclusion of the experiment. Surgical lesions in hypothalamus indicated by two red areas. (b) Parabiotic rats share circulatory system. Rats on the right side of a pair received surgical hypothalamus lesions but ones on the left remained unaltered. (c) Body weight data on individual rat or paired rats after parabiotic surgery, followed by hypothalamic lesion surgery. Parabiotic rats were separated and measured individually at the end of the experiment. Dashed lines are predicted weight changes before separation. Fig. 23.11

Parabiotic Mice & Two Obesity Genes Figure 23.12 Experimental results from wild-type and mutant parabiotic mice. Parabiotic mice in all pair-wise combinations of wt, ob, and db mice. Parabiotic mice lived for several months under free-feeding conditions before the end of the experiment when investigators collected measurements. Fig. 23.12

Table 23.1 compare wt and ob rats Table 23.1 Table 23.1 Effects of exercise on rat body weight and body composition. * Mean values ± standard error of the mean with 6 rats in each group. Different superscript letters within the same column indicate significant differences p < 0.05. Table 23.1

compare wt, ob and db mice Table 23.2 compare wt, ob and db mice Table 23.2 Body weight and percent body fat in free-feeding and pair-fed mutant and wild-type mice. * Mean values ± standard error of the mean with 4 mice in each group. Table 23.2

Cloning and Sequencing ob Gene Figure 23.13 Cloning and sequencing mammalian ob gene, leptin. (a) Aligned amino acid sequences encoded by mouse and human ob genes, called leptin. * indicates differences in amino acids while + indicates a conservative amino acid substitution. Underlined region is the same as in Figure 23.15b. (b) RT-PCR of mRNA isolated from the indicated wt mouse tissues. PCR products for leptin and actin were analyzed on separate gels. (c) Southern blot of Eco RI digested genomic DNA isolated from 12 different animals with leptin cDNA used as probe. Fig. 23.13

Molecular Cause of ob and db Alleles Figure 23.14 Functions of mutant ob alleles in mice. (a) Northern blot of mRNA from the indicated tissue of five different mice produced from two different genetic background strains. Leptin cDNA was used as probe on blot #1 and actin cDNA was used on blot #2. (b) Chromatographs of wt and ob leptin genes as indicated. Numbered amino acids appear above their codons. Fig. 23.14

Functional Verification of Leptin Figure 23.15 Functional tests of leptin protein. Investigators produced mouse leptin protein in bacteria and injected the protein into ob and db mice as indicated. The amount of food mice ate and their body weight was measured periodically for a month. Each point represents the average of 10 animals ± standard deviation. The difference between leptin treated ob mice and the controls was significant p < 0.0001. Fig. 23.15

Leptin Receptor Distribution Figure 23.16 Cloned leptin receptor and tissue distribution. (a) Leptin receptor mRNA is detected on Northern blot using a range of tissues. (b) Axial section of adult rat brain. (c) Radioactive (125I) leptin bound to its receptor and exposed X-ray film as indicated by white portions. The radioactive leptin was incubated with wt and ob rat brains as was a non-radioactive version of leptin. Fig. 23.16

wt and db Gene Structure Figure 23.17 Wild-type and db leptin receptors. Wild-type gene and mRNA for short and long forms of leptin receptor produced by alternative splicing. The db allele contains a 106 bp insertion (yellow) that encodes different amino acids followed by a new stop codon (red). Green indicates coding exons, grey is 3’ untranslated codon, thin lines show alternative splicing patterns, thick red line is the functional stop codon and thin red line is non-functional stop codon. Fig. 23.17

Lipostat Maintains Fat Homeostasis Figure 23.18 Proposed lipostat mechanism for fat homeostasis. Fat mice produce more leptin which causes the mice to lose fat. Skinny mice produce very little leptin which causes them to store more fat. Ob mice produce no functional leptin which causes them to store more fat. Fig. 23.18

Human Variation of Leptin Levels Figure 23.19 Variation in leptin levels. (a) Box and whiskers plot showing variation in daily leptin levels in 25 girls 13 years old; midnight and 4 am were significantly higher p < 0.0001. (b) Graph shows the distribution of average daytime serum leptin levels for each girl as a function of percentage of body fat. Blue line shows the correlation coefficient (r) and black arcs show the 95% confidence interval. (c) Change in peak serum leptin levels as a function change in body fat for the same 25 girls 6 months later. (d) Variation in 13 Pakistanis (blue diamonds) carrying a leptin null allele (DG133) compared to 96 control individuals (orange diamonds) from the same ethnic group; green squares represent homozygous wt blood relatives of the heterozygotes. Fig. 23.19

Leptin Affects More than Fat Figure 23.20 Leptin regulates many aspects of homeostasis. (a) Three groups of 8 male wt rats were treated as indicated and measured for blood pressure and heart rate; * indicates significant difference in blood pressure (p < 0.05). (b) Change in mRNA levels of fat cells isolated from adult male rats two hours after insulin exposure. Fig. 23.20

fertility of ob males +/- leptin injections Table 23.3 fertility of ob males +/- leptin injections Table 23.3 Mouse litter sizes from wt females mated with ob males. Table 23.3 Mouse litter sizes from wt females mated with ob males. Table 23.3

Male Sterility in ob Mice Figure 23.21 Leptin influences male fertility. Wild-type and ob male mice were treated as indicated before isolating testicle tissue for microscopic examination. Sperm cells appear as small dark nuclei surrounded by opaque tissue. Fig. 23.21

High Fat Diets Affects Lipostat Figure ELSI 23.2 High fat foods you can choose, or not. KFC marketed a no-bun, two pieces of chicken, bacon and cheese sandwich. Many state fairs sell fried Twinkies. You can see the commercial advertising a chicken sandwich with bacon, cheese and no bun here (http://www.youtube.com/watch?v=9L1Fhbb8Av0&feature=related). This sandwich has the highest fat content of all KFC products. Fig. ELSI 23.2

Plants Must Survive Environmental Stress Figure 23.22 Plants must tolerate extreme conditions. Since most plants cannot move, they have to respond to stress such as (a) corn during a hot drought, (b) sea oats exposed to heat and high salt, (c) frees under water and (d) grass in a cold snap. Fig. 23.22

Genes Respond to Environmental Stress Figure 23.23 Plant genes respond to environmental stress. (a) Four stress response genes respond differentially to particular stresses. (b) All genes that respond strongly to all five environmental stresses after one hour or twelve hours of continued stress. Each line is a different gene and colors help distinguish individual genes. Fig. 23.23

Correlation of Gene Responses and Time Figure 23.24 Correlation of environment and time for gene responses. Percent overlap of genes that responded to the indicated stresses. Blue area compares 1 hour responses, yellow area compares 12 hour responses and diagonal compares same stresses at 1 hour vs. 12 hours. Shading highlights the range of percent overlap genes. Fig. 23.24

Table 23.4 Table 23.4 Number of genes that responded to only one environmental stress. Table 23.4 Number of genes that responded to only one environmental stress. Table 23.4

Table 23.5 Table 23.5 Current estimated number of genes for plants and animals. Table 23.4 Number of genes that responded to only one environmental stress. Table 23.5

Specific Responses to Stresses Figure 23.25 Tissue and time specific responses to environmental stress. Investigators quantified genes that were induced or repressed by 2 fold or more in leaves and roots after either 3 hours or 27 hours of treatment. Venn diagrams show overlap of gene expression as indicated. Fig. 23.25

Homeostasis of Apple Genome Figure 23.26 Golden delicious apple genome analysis. (a) The golden delicious apple is the product of selective breeding to optimize taste. (b) Dot plots compare two apple chromosomes to reveal syntenic regions. Chromosomes 7 and 13 served as a negative control comparison. Fig. 23.26

Evolutionary History of Apple Genome Figure 23.27 Deduced apple genome duplication and karyotype. Ancestral genome duplicated about 50 million years ago and since them chromosomes have fragmented, fused and evolved. Colors show syntenic regions, white shows area of no sequence similarity, red/white hatching indicates low sequence conservation. Fig. 23.27

Tetraploid Plants from Diploid Parents Figure 23.28 Synthetic tetraploid hybrids and their progeny. (a) All the plants are naturally occurring species except for the one synthetic tetraploid produced only in the lab. (b) Parental species are above and eight synthetic tetraploid progeny are below. Pink box surrounds plants derived from T. porrifolius ovules and T. dubius pollen; yellow are products of the reciprocal cross. (c) Parental species are above and eight synthetic tetraploid progeny are below. As in panel b, pink and yellow boxes indicate the color of the flower used for the ovules. Fig. 23.28

Non-Random Inhibition of Alleles Figure 23.29 G3P dehydrogenase non-random gene alterations. (a) G3P dehydrogenase cDNA characterization from naturally produced T. mirus plants and nearby parental stocks. Red arrows indicate alleles still present in genome but not transcribed; white arrows denote alleles deleted from genome. (b) Similar analysis for independent T. mirus and parental stocks from two different sites in the (c) adjacent towns western Washington towns of Pullman and Palouse. Fig. 23.29