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CELL MEMBRANE Fructose [b] Glucose [b] [a] Maltose Glucose [1] ATP ADP P i Fructose ATP [c] Glucose 6-P [2] Glucose 1-P [e] Glycogen [d] ADP Fructose 6-P PP i [3] P i Dihydroxyacetone-P [v] sn-Glycerol 3-P [5] Fructose 1,6-bisP [4] Glyceraldehyde 3-P [6] 1,3-bisP-Glycerate ADP [w] P i [7] ATP Glycerol 3-P-Glycerate [8] 2-P-Glycerate [9] P-enolpyruvate FIGURE 7.1 Map of the entry of hexoses into glycolysis and the process through the formation of phosphoenolpyruvate. Fate of reducing equivalents omitted. Metabolic end-products boxed. [a] -Glucosidase, [b] hexose transporter, [c] fructokinase (Tr. foetus only), [d] glycogen phosphorylase, [e] phosphoglucomutase, [1] glucokinase, [2] glucosephosphate isomerase, [3] phosphofructokinase (PP i -dependent), [4] fructose bisphosphate aldolase, [5] triosephosphate isomerase, [6] glyceraldehyde 3-phosphate dehydrogenase, [7] 3-glycerophosphate kinase, [8] 3- glycerophosphate mutase, [9] enolase, [v] glycerolphosphate dehydrogenase (T. vaginalis only), [w] glycerolphosphate phosphatase (T. vaginalis only). (Figures modified from illustrations in the first edition of this work.)
130 ENERGY METABOLISM – ANAEROBIC PROTOZOA Conversion of triosephosphates into phosphoenolpyruvate Dihydroxyacetone phosphate and glyceraldehyde 3-phosphate are kept in equilibrium through the action of triosephosphate isomerase [reaction 5]. Glyceraldehyde 3-phosphate dehydrogenase [reaction 6], 3- phosphoglycerate kinase [reaction 7], 3-phosphoglycerate mutase [reaction 8], and enolase [reaction 9] convert glyceraldehyde 3-phosphate to phosphoenolpyruvate (PEP). The triosephosphates represent the first branch-point of fermentation, since an alternative path leads from dihydroxyacetone phosphate to glycerol, a metabolic end-product arising through the successive actions of glycerolphosphate dehydrogenate [reaction v] and glycerolphosphate phosphatase [reaction w], a process detected in T. vaginalis, but not in E. histolytica. Further conversions of phosphoenolpyruvate PEP is the central, key intermediate of carbohydrate catabolism. PEP and its metabolites can be processed in different directions; thus several branch-points of metabolism are present in the pathways downstream of PEP. While Type I and Type II amitochondriates differ significantly in the processes leading from PEP to the dominant metabolic end-products and in their subcellular location, there are several common features as well (Figures 7.2 and 7.3). A main pathway leads to pyruvate by the action of pyruvate kinase [reaction 10] and/or pyruvate, orthophosphate dikinase (pyruvate dikinase) [reaction 11]. Interestingly, the presence of these enzymes is species dependent. G. intestinalis contains both activities, E. histolytica has only pyruvate dikinase, T. vaginalis carries pyruvate kinase, and so far neither enzyme has been detected in Tr. foetus. A large part of the pyruvate is subsequently processed to acetyl-CoA, as discussed below in the section on the enzymatic differences between amitochondriate and mitochondriate cells. A putative alternative fate of PEP is carboxylation to oxalacetate [reaction 12 or 13] (Figures 7.2 and 7.3). Oxalacetate can be reduced by malate dehydrogenase [reaction 14] to malate, which in turn can be oxidatively decarboxylated to pyruvate by malate dehydrogenase (decarboxylating) or ‘malic enzyme’ [reaction 15]. In essence, this sequence of reactions represents a possible bypass to the pyruvate kinase/pyruvate dikinase reaction. Oxalacetate probably enters other pathways that remain to be identified. In Tr. foetus, cytosolic fumarate hydratase [reaction x) and fumarate reductase (reaction y) reduce oxalacetate to succinate (Figure 7.3), which is released as a metabolic end-product. The most significant differences between Type I and Type II amitochondriates are in the metabolic steps beyond pyruvate (Figures 7.2 and 7.3). In Type I organisms all steps take place in the cytosol (Figure 7.2). Pyruvate can be transaminated to alanine [reaction 16] or oxidatively decarboxylated [reaction 17]. Acetyl- CoA formed in the latter reaction is converted either to acetate or ethanol. Acetate formation is catalyzed by a single enzyme, acetyl-CoA synthetase (ADP-forming) accompanied by substrate-level phosphorylation [reaction 18]. Ethanol is produced by the action of a fused NAD-specific aldehyde/alcohol dehydrogenase [reaction 19]. In eukaryotes, these two enzymes have been found so far only in Type I amitochondriates. Reducing equivalents produced in pyruvate oxidation are transferred to ferredoxin. The mechanism of the reoxidation of ferredoxin remains unknown, though it is likely that the reducing equivalents are used in ethanol production. Linking ferredoxin to ethanol BIOCHEMISTRY AND CELL BIOLOGY: PROTOZOA
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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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Page 92 and 93: POST-TRANSCRIPTIONAL REGULATION IN
Page 100 and 101: FURTHER READING 87 inhibition, it m
Page 102 and 103: C H A P T E R 5 Antigenic variation
Page 104 and 105: ANTIGENIC VARIATION AT THE STRUCTUR
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Page 108 and 109: VSG Signal sequence Amino-terminal
Page 110 and 111: GENETICS OF ANTIGENIC VARIATION 97
Page 116 and 117: IMMUNE RESPONSES TO TRYPANOSOME INF
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Page 122 and 123: FURTHER READING 109 ACKNOWLEDGEMENT
Page 124 and 125: C H A P T E R 6 Genetic and genomic
Page 126 and 127: ‘FORWARD’ VS. ‘REVERSE’ GEN
Page 128 and 129: EXAMPLES OF ‘FORWARD’ GENETIC A
Page 130 and 131: EXAMPLES OF ‘FORWARD’ GENETIC A
Page 132 and 133: REVERSE GENETICS AND LEISHMANIA VIR
Page 134 and 135: VALIDATION OF CANDIDATE VIRULENCE G
Page 136 and 137: S E C T I O N II BIOCHEMISTRY AND C
Page 138 and 139: C H A P T E R 7 Energy metabolism P
Page 140 and 141: SUBCELLULAR ORGANIZATION OF AMITOCH
Page 144 and 145: STEPS OF AMITOCHONDRIATE CORE METAB
Page 146 and 147: ENZYMATIC DIFFERENCES BETWEEN AMITO
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Page 150 and 151: ENVOI 137 unambiguously reflect the
Page 152 and 153: FURTHER READING 139 Saavedra-Lira,
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Page 164 and 165: WHY DO TRYPANOSOMATIDAE HAVE GLYCOS
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Page 168: CARBOHYDRATE METABOLISM 155 as a hu
Page 171 and 172: 158 ENERGY METABOLISM - APICOMPLEXA
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Page 185 and 186: 172 PROTEIN METABOLISM PROTEINS (1)
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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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298 HELMINTH SURFACES Important exc
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300 HELMINTH SURFACES protease inhi
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302 HELMINTH SURFACES volume, there
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304 HELMINTH SURFACES projecting si
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306 HELMINTH SURFACES schistosome t
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308 HELMINTH SURFACES re-establish
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310 HELMINTH SURFACES hepatic cells
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312 HELMINTH SURFACES lungs. Larvae
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314 HELMINTH SURFACES cuticle, whic
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316 HELMINTH SURFACES cuticle in th
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318 HELMINTH SURFACES mec-8 or sym-
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320 HELMINTH SURFACES current, when
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322 HELMINTH SURFACES The cuticle-h
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324 HELMINTH SURFACES are typically
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326 HELMINTH SURFACES or carrier pr
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328 HELMINTH SURFACES of tyrosine-b
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330 HELMINTH SURFACES blood. The ge
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332 HELMINTH SURFACES Mutations in
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334 HELMINTH SURFACES in the hypode
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336 HELMINTH SURFACES (including H-
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338 HELMINTH SURFACES Blaxter, M.L.
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340 ENERGY METABOLISM IN HELMINTHS
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360 NEUROTRANSMITTERS CO 2 H NH 2 G
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362 NEUROTRANSMITTERS TABLE 15.1 An
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364 NEUROTRANSMITTERS more arms tha
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366 NEUROTRANSMITTERS the surroundi
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368 NEUROTRANSMITTERS proteins requ
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370 NEUROTRANSMITTERS FIGURE 15.11
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372 NEUROTRANSMITTERS FIGURE 15.13
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374 NEUROTRANSMITTERS sensitivity t
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376 NEUROTRANSMITTERS TABLE 15.3 Cl
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378 NEUROTRANSMITTERS crossed the c
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380 NEUROTRANSMITTERS have been tes
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382 NEUROTRANSMITTERS C-terminals a
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384 NEUROTRANSMITTERS Davis and Str
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386 NEUROTRANSMITTERS Cephalic gang
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388 NEUROTRANSMITTERS myoexcitation
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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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