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GLYCOLYSIS 341 fluctuate between periods of glycogen degradation and synthesis, and the replenishment of glycogen reserves is not induced by a marked decrease in the glycogen levels, but instead occurs slowly and continuously. Therefore, the role of the glycogen metabolism in blooddwelling parasites like adult schistosomes, that continuously reside in glucose-rich environments, is still not clear. Since the replenishment of the endogenous glycogen reserves in adult S. mansoni is not induced by a marked decrease in the glycogen levels, but occurs slowly in vivo and continuously in each and every worm pair, it is likely that glycogen is degraded intermittently, for instance for muscle contraction or tegumental membrane repair. This metabolism of glucose ‘through’ glycogen could help to maintain a low internal free glucose pool and so promote sufficient glucose import to deeper tissues through diffusion. In this respect it is noteworthy that adult schistosomes exhibit relatively high glucose 6-phosphatase activity, which would allow glucose derived from degraded glycogen stores in one cell to be exported to other cells within the adult. A balance between the rate of phosphorylation of imported glucose by hexokinase and the rate of glucose released from internal glycogen stores by glucose 6-phosphatase may help maintain an even distribution of glucose throughout the worm, and promote continuous, energyindependent movement of free glucose into the worm down a concentration gradient. Trehalose is a soluble -1-linked nonreducing disaccharide of glucose, and in many parasitic nematodes is more abundant than glucose. Trehalose is synthesized by the combined action of trehalose 6-phosphate synthase and trehalose 6-phosphate phosphatase, and is degraded to glucose by the action of trehalase. These enzymes have been detected in parasitic nematodes, but not extensively characterized. Trehalose levels are usually lower than those of glycogen, but trehalose still may function as a critical carbohydrate reserve in many nematodes and their eggs. However, since the storage of glycogen is energetically more favorable than trehalose, many authors have suggested that trehalose might also serve as an intermediate in glusose <strong>trans</strong>port to the tissues, as has been well documented in insects. Trehalose is also clearly involved in stress responses in many nematodes, and may be important in resistance to desiccation and in cryoprotection. GLYCOLYSIS Glycolysis is the degradation of glucose to yield two molecules of pyruvate, and this almost universal pathway is also used by parasitic helminths for the catabolism of glucose, their main substrate for energy generation. Glycolysis occurs in the cytosol, and the compartmentalization of glycolytic enzymes within a membrane-bound organelle, like the glycosomes of some protozoan parasites, has not been observed in parasitic helminths. Based on the end-products of the glycolytic pathway and their further metabolism, parasitic helminths can be classified into three types: 1. Those parasitic helminths that use the complete glycolytic pathway and export the endproduct, pyruvate, into the mitochondria for further degradation via the tricarboxylic acid cycle. This aerobic degradation occurs mainly in larval stages of cestodes, trematodes and nematodes (see section on the Aerobic/Anaerobic Transition). 2. Those that use the complete glycolytic pathway, but cytoplasmically convert its end-product, pyruvate, to more reduced end-products such as lactate and ethanol. This fermentation process, so-called BIOCHEMISTRY AND CELL BIOLOGY: HELMINTHS
342 ENERGY METABOLISM IN HELMINTHS FIGURE 14.1 Glycogenolysis and glycolysis in parasitic helminths. (1) glycogen phosphorylase; (2) glycogen synthase; (3) phosphoglucomutase; (4) hexokinase; (5) glucosephosphate isomerase; (6) phosphofructokinase; (7) aldolase; (8) triosephosphate isomerase; (9) glyceraldehyde-3-P dehydrogenases; (10) phosphoglycerate kinase; (11) phosphoglyceromutase; (12) enolase; (13) pyruvate kinase; (14) lactate dehydrogenase; (15) phosphoenolpyruvate carboxykinase; (16) malate dehydrogenase. ‘anaerobic’ glycolysis, occurs in adult schistosomes and filarial nematodes. 3. Those that use the classical glycolytic pathway only up to phosphoenolpyruvate (PEP). Then instead of converting PEP to pyruvate, PEP is carboxylated by PEP carboxykinase (PEPCK) to oxaloacetate, which is subsequently reduced to malate (Figure 14.1). This part of the pathway occurs in the cytosol and is comparable to the formation of lactate or BIOCHEMISTRY AND CELL BIOLOGY: HELMINTHS
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Molecular Medical Parasitology
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Molecular Medical Parasitology Edit
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Contents List of contributors Prefa
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List of contributors Mark Blaxter,
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LIST OF CONTRIBUTORS ix Richard. J.
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Preface Parasitology was born as th
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S E C T I O N I MOLECULAR BIOLOGY
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C H A P T E R 1 Parasite genomics M
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TABLE 1.1 Parasite genomes: genome
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GENERATING GENOMICS DATA 7 differen
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GENERATING GENOMICS DATA 9 TABLE 1.
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GENERATING GENOMICS DATA 11 called
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GENERATING GENOMICS DATA 13 200 000
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BIOINFORMATICS AND THE ANALYSIS OF
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THE POST-GENOMICS ERA, AND THE OTHE
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THE PARASITES AND THEIR GENOMES 19
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FURTHER READING 27 treated with a d
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C H A P T E R 2 RNA processing in p
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TRANS-SPLICING 31 cis trans Exon 1
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TRANS-SPLICING 33 snRNPs (small nuc
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TRANS-SPLICING 35 trans cis U2AF35
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RNA EDITING 37 P AAAA... AAAA... AA
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RNA EDITING 39 entire transcript re
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RNA EDITING 41 5 Editing block C Ed
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RNA EDITING 43 microscopy) approach
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FURTHER READING 45 Nilsen, T.W. (19
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C H A P T E R 3 Transcription Arthu
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UNUSUAL MODES OF TRANSCRIPTION IN T
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CLASS I TRANSCRIPTION IN TRYPANOSOM
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CLASS II TRANSCRIPTION OF PROTEIN C
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SL RNA AND U snRNA GENE TRANSCRIPTI
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FURTHER READING 65 and switching in
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C H A P T E R 4 Post-transcriptiona
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POST-TRANSCRIPTIONAL REGULATION IN
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FURTHER READING 87 inhibition, it m
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C H A P T E R 5 Antigenic variation
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ANTIGENIC VARIATION AT THE STRUCTUR
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ANTIGENIC VARIATION AT THE STRUCTUR
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VSG Signal sequence Amino-terminal
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GENETICS OF ANTIGENIC VARIATION 97
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IMMUNE RESPONSES TO TRYPANOSOME INF
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INNATE RESISTANCE, HUMAN SUSCEPTIBI
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ANTIGENIC VARIATION IN MALARIA 107
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FURTHER READING 109 ACKNOWLEDGEMENT
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C H A P T E R 6 Genetic and genomic
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‘FORWARD’ VS. ‘REVERSE’ GEN
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EXAMPLES OF ‘FORWARD’ GENETIC A
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EXAMPLES OF ‘FORWARD’ GENETIC A
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REVERSE GENETICS AND LEISHMANIA VIR
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VALIDATION OF CANDIDATE VIRULENCE G
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S E C T I O N II BIOCHEMISTRY AND C
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C H A P T E R 7 Energy metabolism P
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SUBCELLULAR ORGANIZATION OF AMITOCH
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CELL MEMBRANE Fructose [b] Glucose
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STEPS OF AMITOCHONDRIATE CORE METAB
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ENZYMATIC DIFFERENCES BETWEEN AMITO
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ACTION OF NITROIMIDAZOLE DRUGS 135
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ENVOI 137 unambiguously reflect the
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FURTHER READING 139 Saavedra-Lira,
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THE EMBDEN-MEYERHOF-PARNAS (EMP) PA
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WHY DO TRYPANOSOMATIDAE HAVE GLYCOS
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FURTHER READING 153 for use in agri
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CARBOHYDRATE METABOLISM 155 as a hu
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158 ENERGY METABOLISM - APICOMPLEXA
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172 PROTEIN METABOLISM PROTEINS (1)
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174 PROTEIN METABOLISM the C-termin
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176 PROTEIN METABOLISM and also, to
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178 PROTEIN METABOLISM values rangi
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180 PROTEIN METABOLISM of the plasm
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182 PROTEIN METABOLISM in vivo, in
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184 PROTEIN METABOLISM PROLINE Poly
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186 PROTEIN METABOLISM CO 2 Dec-SAM
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188 PROTEIN METABOLISM a cMDH has b
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190 PROTEIN METABOLISM Urea ARGININ
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192 PROTEIN METABOLISM been describ
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194 PROTEIN METABOLISM absence of g
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198 PURINES AND PYRIMIDINES enable
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200 PURINES AND PYRIMIDINES provide
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202 PURINES AND PYRIMIDINES activit
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204 PURINES AND PYRIMIDINES physiol
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206 PURINES AND PYRIMIDINES Amitoch
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208 PURINES AND PYRIMIDINES their a
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210 PURINES AND PYRIMIDINES FIGURE
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214 PURINES AND PYRIMIDINES protein
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220 PURINES AND PYRIMIDINES in Plas
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222 PURINES AND PYRIMIDINES whereas
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226 TRYPANOSOMATID CARBOHYDRATES AF
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228 TRYPANOSOMATID CARBOHYDRATES In
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230 TRYPANOSOMATID CARBOHYDRATES po
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232 TRYPANOSOMATID CARBOHYDRATES LP
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234 TRYPANOSOMATID CARBOHYDRATES re
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236 TRYPANOSOMATID CARBOHYDRATES sc
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A. sAP COOH [T][T](S/T)(S/T)(S/T)SS
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240 TRYPANOSOMATID CARBOHYDRATES Cr
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242 INTRACELLULAR SIGNALING protein
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244 INTRACELLULAR SIGNALING FIGURE
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246 INTRACELLULAR SIGNALING 212.5 2
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248 INTRACELLULAR SIGNALING cycle.
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250 INTRACELLULAR SIGNALING V-H -A
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252 INTRACELLULAR SIGNALING domain)
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254 INTRACELLULAR SIGNALING the kno
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256 INTRACELLULAR SIGNALING from in
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258 INTRACELLULAR SIGNALING FIGURE
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260 INTRACELLULAR SIGNALING ESAG4 (
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262 INTRACELLULAR SIGNALING and ind
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264 INTRACELLULAR SIGNALING ATPase
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266 INTRACELLULAR SIGNALING G11XG
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268 INTRACELLULAR SIGNALING a diffe
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270 INTRACELLULAR SIGNALING rapid l
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272 INTRACELLULAR SIGNALING cells w
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274 INTRACELLULAR SIGNALING PfPPJ i
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276 INTRACELLULAR SIGNALING is cont
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278 PLASTIDS, MITOCHONDRIA, AND HYD
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Page 303 and 304: 290 PLASTIDS, MITOCHONDRIA, AND HYD
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Page 311 and 312: 298 HELMINTH SURFACES Important exc
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Page 315 and 316: 302 HELMINTH SURFACES volume, there
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Page 319 and 320: 306 HELMINTH SURFACES schistosome t
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Page 325 and 326: 312 HELMINTH SURFACES lungs. Larvae
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Page 349 and 350: 336 HELMINTH SURFACES (including H-
Page 351 and 352: 338 HELMINTH SURFACES Blaxter, M.L.
Page 353: 340 ENERGY METABOLISM IN HELMINTHS
Page 357 and 358: 344 ENERGY METABOLISM IN HELMINTHS
Page 373 and 374: 360 NEUROTRANSMITTERS CO 2 H NH 2 G
Page 375 and 376: 362 NEUROTRANSMITTERS TABLE 15.1 An
Page 377 and 378: 364 NEUROTRANSMITTERS more arms tha
Page 379 and 380: 366 NEUROTRANSMITTERS the surroundi
Page 381 and 382: 368 NEUROTRANSMITTERS proteins requ
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Page 385 and 386: 372 NEUROTRANSMITTERS FIGURE 15.13
Page 387 and 388: 374 NEUROTRANSMITTERS sensitivity t
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Page 395 and 396: 382 NEUROTRANSMITTERS C-terminals a
Page 397 and 398: 384 NEUROTRANSMITTERS Davis and Str
Page 399 and 400: 386 NEUROTRANSMITTERS Cephalic gang
Page 401 and 402: 388 NEUROTRANSMITTERS myoexcitation
Page 403 and 404: 390 NEUROTRANSMITTERS is phosphoryl
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392 NEUROTRANSMITTERS many other an
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398 DRUG RESISTANCE of some of the
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400 DRUG RESISTANCE It is now estim
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402 DRUG RESISTANCE is again assume
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404 DRUG RESISTANCE An alternative
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406 DRUG RESISTANCE clinical eviden
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408 DRUG RESISTANCE FIGURE 16.4 Fol
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410 DRUG RESISTANCE Using similar s
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412 DRUG RESISTANCE whether these r
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414 DRUG RESISTANCE FIGURE 16.5 Str
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416 DRUG RESISTANCE FIGURE 16.6 Try
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418 DRUG RESISTANCE has permitted e
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420 DRUG RESISTANCE FIGURE 16.7 Dru
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422 DRUG RESISTANCE near future. Th
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424 DRUG RESISTANCE million new inf
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426 DRUG RESISTANCE some 50 million
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428 DRUG RESISTANCE pharynx, the bo
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430 DRUG RESISTANCE efforts for glo
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432 DRUG RESISTANCE and resistance
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434 MEDICAL IMPLICATIONS TABLE 17.1
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436 MEDICAL IMPLICATIONS TABLE 17.1
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438 MEDICAL IMPLICATIONS transmissi
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440 MEDICAL IMPLICATIONS H 2 C H H
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442 MEDICAL IMPLICATIONS parasites
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444 MEDICAL IMPLICATIONS neuropsych
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446 MEDICAL IMPLICATIONS of toxic f
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448 MEDICAL IMPLICATIONS Future con
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450 MEDICAL IMPLICATIONS Melarsopro
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452 MEDICAL IMPLICATIONS prevention
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454 MEDICAL IMPLICATIONS resulting
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456 MEDICAL IMPLICATIONS for S. ste
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458 MEDICAL IMPLICATIONS are though
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460 MEDICAL IMPLICATIONS FIGURE 17.
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462 MEDICAL IMPLICATIONS Marr, J.J.
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464 INDEX Aldolase, 143 Plasmodium
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466 INDEX Ascofuranone, 143 ASCUT-1
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468 INDEX Cnidarians, RNA trans-spl
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470 INDEX Entamoeba, 125 Ca 2 metab
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472 INDEX Glucose-6-phosphate dehyd
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474 INDEX Ivermectin, 398, 427, 455
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476 INDEX Maduramicin, 412 Major va
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478 INDEX Nitric oxide: neurotransm
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480 INDEX calcium-binding proteins,
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482 INDEX Pyrimidine transport, 200
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484 INDEX Succinate:rhodoquinone ox
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486 INDEX genome, 21 survey sequenc
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488 INDEX U small nuclear RNA (snRN
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