53:
125:(CMS). CMS occurs in many plants. mtDNA mutations are responsible for this phenomenon. However, nuclear restorer genes (Rf or Fr) could infer male fertility. Therefore, interaction between mtDNA and nuclear genes could be one of mechanisms that counteract deleterious effects of male-specific mtDNA mutations
145:
Mitochondria play a pivotal role in eukaryotic respiration. Because of maternal inheritance, mtDNA has no selection in males. Instead, mutations only deleterious to males could be maintained and reach a higher frequency by selection or genetic drift in females. As a consequence, asymmetric effects of
66:
Mother's curse predicts that mtDNA mutations pose a greater threat on males and male-specific detrimental mutations in mtDNA could be maintained and reach a high frequency. Several researches support these predictions. In humans, a mtDNA haplogroup that exhibits reduction in sperm mobility reaches a
56:
The process showing how mother's curse occurs. mtDNA mutates and generates copies that are detrimental for females (red) and copies that only detrimental for males (blue). Mitochondria bad for females are selected against, while mitochondria only bad for males are transmitted to the offspring. As a
31:
As mtDNA is usually maternally inherited, mtDNA mutations deleterious to males but beneficial, neutral or less deleterious to females are not subjected to be selected against, which results in a sex-biased selective sieve. Therefore, male-specific deleterious mtDNA mutations could be maintained and
106:
If mtDNA mutations deleterious to male fitness could not be selected against, they would reach a high frequency despite the high fitness cost for males. Eventually, detrimental mutations would be fixed and lead to species extinction. However, we have not observed extinction in spite of high
118:– Although mtDNA is thought to be exclusively maternally inherited, paternal inheritance exists in a low frequency of 10 relative to maternal inheritance in mice. Hence, selection can act on male-specific deleterious mutations when they are paternally inherited, decreasing their frequency.
49:(LHON) is caused by one or several point mutations on mtDNA and LHON affects more males than females. In mice, a deletion on mtDNA causes oligospermia and asthenozoospermia, resulting in infertility. Taken together, mtDNA mutations pose a greater threat on males than on females.
44:
Males are more susceptible to mtDNA defects, not only because of lack of selection for mtDNA on males but also due to sperm's higher energy requirements for motility. There are evidence showing mtDNA mutations are more likely to affect males. In humans,
313:
Dowling, Damian K., A. Larkeson
Nowostawski, and Göran Arnqvist. "Effects of cytoplasmic genes on sperm viability and sperm morphology in a seed beetle: implications for sperm competition theory?." Journal of Evolutionary Biology 20.1 (2007):
93:
analyzed two different haplotype of mtDNA in hares and found that males of those two haplogroups show variation in their reproductive success. In addition, the mitochondrial genome is associated with sperm viability and length in seed beetles
215:
Smith, Steve, Christopher
Turbill, and Franz Suchentrunk. "Introducing mother's curse: low male fertility associated with an imported mtDNA haplotype in a captive colony of brown hares." Molecular ecology 19.1 (2010):
40:
and population viability. In addition, the effect of mtDNA mutations on fitness has a threshold effect, i.e. only when the number of mutation reaches the threshold, mtDNA mutations will decrease individual fitness.
244:
Labuda, Damian; Brais, Bernard; Alan A. Cohen; Gagnon, Alain; Moreau, Claudia; Milot, Emmanuel (September 2017). "Mother's curse neutralizes natural selection against a human genetic disease over three centuries".
88:
lines with isogenic nuclear genome and different mtDNA haplotypes. They demonstrated that mtDNA polymorphism is responsible for male aging, while there is no significant effect on female longevity. Smith
295:
Innocenti, Paolo, Edward H. Morrow, and Damian K. Dowling. "Experimental evidence supports a sex-specific selective sieve in mitochondrial genome evolution." Science 332.6031 (2011): 845-848.
225:
Riordan-Eva, P., et al. "The clinical features of Leber's hereditary optic neuropathy defined by the presence of a pathogenic mitochondrial DNA mutation." Brain 118.2 (1995): 319-337.
332:
Schnable, Patrick S., and Roger P. Wise. "The molecular basis of cytoplasmic male sterility and fertility restoration." Trends in plant science 3.5 (1998): 175-180.
146:
mtDNA mutations result in sexual conflict. On the other hand, to alleviate the effect of mother's curse, interaction between mtDNA and nuclear genes promotes
304:
Camus, M. Florencia, David J. Clancy, and Damian K. Dowling. "Mitochondria, maternal inheritance, and male aging." Current
Biology 22.18 (2012): 1717-1721.
80:, mtDNA polymorphism mainly affects nuclear gene expression in males but not in females and those genes are predominantly male-biased. Moreover, Camus e
341:
Wade, Michael J., and Yaniv
Brandvain. "Reversing mother's curse: selection on male mitochondrial fitness effects." Evolution 63.4 (2009): 1084-1089.
371:
203:. "Mother's curse: the effect of mtDNA on individual fitness and population viability." Trends in Ecology & Evolution 19.5 (2004): 238-244.
68:
46:
234:
Nakada, Kazuto, et al. "Mitochondria-related male infertility." Proceedings of the
National Academy of Sciences 103.41 (2006): 15148-15153.
136:
could also relieve fitness cost of male-specific deleterious mtDNA mutations, while negative assortative mating has an opposite function.
111:
of mtDNA. So there must be ways that species could decrease the effects of male-specific deleterious mtDNA mutations.
115:
366:
122:
76:
376:
182:
278:
129:
28:
from their mother, while those mutations are beneficial, neutral or less deleterious to females.
270:
262:
200:
37:
323:
Gyllensten, Ulf, et al. "Paternal inheritance of mitochondrial DNA in mice." (1991): 255-257.
254:
159:
67:
frequency of 20%. A 2017 study found the mother's curse preserving a mutation that causes
350:
Hedrick, Philip W. "Reversing mother's curse revisited." Evolution 66.2 (2012): 612-616.
360:
133:
108:
21:
57:
result, the males of offspring who inherit bad mutations would have a lower fitness.
282:
147:
33:
258:
266:
25:
274:
102:
How to counteract the effects of male-specific deleterious mtDNA mutations
52:
51:
121:
Interaction between mtDNA and nuclear genome – A good example is
20:
is an evolutionary effect that males inherit deleterious
71:
in a population of French
Canadians for over 290 years.
183:"Evolution: mitochondrial burden on male health."
8:
199:Gemmell, Neil J., Victoria J. Metcalf, and
185:Current Biology 22.18 (2012): R797-R799.
211:
209:
177:
175:
171:
195:
193:
191:
150:of mitochondrial and nuclear genomes.
7:
69:Leber's hereditary optic neuropathy
47:Leber's hereditary optic neuropathy
14:
247:Nature Ecology & Evolution
1:
372:Evolutionary biology concepts
393:
141:Significance for evolution
123:cytoplasmic male sterility
32:reach a high frequency in
259:10.1038/s41559-017-0276-6
96:Callosobruchus maculatus
77:Drosophila melanogaster
58:
55:
36:, decreasing males'
130:assortative mating
59:
367:Genetics concepts
201:Fred W. Allendorf
181:Frank, Steven A.
384:
351:
348:
342:
339:
333:
330:
324:
321:
315:
311:
305:
302:
296:
293:
287:
286:
253:(9): 1400–1406.
241:
235:
232:
226:
223:
217:
213:
204:
197:
186:
179:
116:Paternal leakage
392:
391:
387:
386:
385:
383:
382:
381:
357:
356:
355:
354:
349:
345:
340:
336:
331:
327:
322:
318:
312:
308:
303:
299:
294:
290:
243:
242:
238:
233:
229:
224:
220:
214:
207:
198:
189:
180:
173:
168:
160:Sexual conflict
156:
143:
104:
86:D. melanogaster
84:constructed 13
64:
24:genome (mtDNA)
12:
11:
5:
390:
388:
380:
379:
374:
369:
359:
358:
353:
352:
343:
334:
325:
316:
306:
297:
288:
236:
227:
218:
205:
187:
170:
169:
167:
164:
163:
162:
155:
152:
142:
139:
138:
137:
126:
119:
103:
100:
63:
60:
18:mother's curse
13:
10:
9:
6:
4:
3:
2:
389:
378:
375:
373:
370:
368:
365:
364:
362:
347:
344:
338:
335:
329:
326:
320:
317:
310:
307:
301:
298:
292:
289:
284:
280:
276:
272:
268:
264:
260:
256:
252:
248:
240:
237:
231:
228:
222:
219:
212:
210:
206:
202:
196:
194:
192:
188:
184:
178:
176:
172:
165:
161:
158:
157:
153:
151:
149:
140:
135:
134:kin selection
131:
127:
124:
120:
117:
114:
113:
112:
110:
109:mutation load
101:
99:
97:
92:
87:
83:
79:
78:
72:
70:
61:
54:
50:
48:
42:
39:
35:
29:
27:
23:
22:mitochondrial
19:
377:Mitochondria
346:
337:
328:
319:
309:
300:
291:
250:
246:
239:
230:
221:
144:
105:
95:
90:
85:
81:
75:
73:
65:
43:
30:
17:
16:In biology,
15:
148:coevolution
34:populations
361:Categories
166:References
267:2397-334X
128:Positive
26:mutations
314:358-368.
275:29046555
154:See also
62:Evidence
283:4183585
38:fitness
281:
273:
265:
216:36-43.
91:et al.
279:S2CID
82:t al.
271:PMID
263:ISSN
132:and
255:doi
98:).
74:In
363::
277:.
269:.
261:.
249:.
208:^
190:^
174:^
285:.
257::
251:1
94:(
Text is available under the Creative Commons Attribution-ShareAlike License. Additional terms may apply.
