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1 y observed association between herkogamy and inbreeding depression.
2 endosperm imprinting, hybrid phenotypes and inbreeding depression.
3 ly recessive deleterious alleles will reduce inbreeding depression.
4 The advantage is inversely related to local inbreeding depression.
5 es with long generation intervals and severe inbreeding depression.
6 tilization selection, and/or the severity of inbreeding depression.
7 ul tool to study the genetic architecture of inbreeding depression.
8 srupting self-incompatibility and leading to inbreeding depression.
9 while simultaneously estimating sex-specific inbreeding depression.
10 ns and may contribute substantially to total inbreeding depression.
11 d not appreciably diminish overall levels of inbreeding depression.
12 igh levels of selfing in plants despite high inbreeding depression.
13 or inviable, sl-CSD can generate substantial inbreeding depression.
14 of floral size expressed highly significant inbreeding depression.
15 lations have rendered the species at risk of inbreeding depression.
16 system itself in response to such factors as inbreeding depression.
17 he relationship between prior inbreeding and inbreeding depression.
18 ficient, revealing direct, but not indirect, inbreeding depression.
19 fects on viability, are contributing to this inbreeding depression.
20 to strong genetic drift and at high risk of inbreeding depression.
21 als dynamic genome evolution and hotspots of inbreeding depression.
22 aphroditic selfing rates and the strength of inbreeding depression.
23 ay express recessive genetic load and suffer inbreeding depression.
24 S-linked genetic load compared with overall inbreeding depression.
25 itland approach for field-based estimates of inbreeding depression.
26 s sizes, and to estimate the power to detect inbreeding depression.
27 which estimate of F is optimal for detecting inbreeding depression.
28 nservation and ecology, such as the study of inbreeding depression.
29 opulations may be subject to consequences of inbreeding depression.
30 alleles, supporting the dominance theory of inbreeding depression.
31 pulation numbers, and reverse indications of inbreeding depression.
32 nd elsewhere, and there was some evidence of inbreeding depression.
36 e detected: (i) variation in reproduction or inbreeding depression among life stages, years and mater
38 on the relationship between the magnitude of inbreeding depression and environmental stress and calcu
39 find strong support for interactions between inbreeding depression and environmental variation compar
40 pports the dominance theory of heterosis and inbreeding depression and establishes the oyster as an a
49 etic selection for the joint distribution of inbreeding depression and mating system across species.
51 rare plants with mixed-mating systems, where inbreeding depression and pollinator scarcity may both c
52 f these evolutionary factors on the level of inbreeding depression and provides an approach that coul
54 species may be particularly at risk because inbreeding depression and stochastic fluctuations in mal
56 anscription play a role in hybrid vigour and inbreeding depression, and also in the absence of parent
57 scue in facilitating adaptation and reducing inbreeding depression, and suggest that demographic resc
58 luding the rate of adaptation, the extent of inbreeding depression, and the load of deleterious mutat
60 that the deleterious effects of inbreeding (inbreeding depression) are expected to be more pronounce
62 recessive alleles are the primary source of inbreeding depression, as does its late expression in bo
64 ergence at the range limit, suggesting local inbreeding depression at both range limit populations; h
65 ought to increase relative female fitness is inbreeding depression avoidance, the magnitude of which
67 terious alleles can lead to large amounts of inbreeding depression because of their high equilibrium
69 reting the genetic basis of the variation in inbreeding depression by: (1) predicting the variation i
70 depression." There is mounting evidence that inbreeding depression can be exacerbated by environmenta
72 dicts that, at equilibrium, the magnitude of inbreeding depression caused by recessive alleles should
73 such as variation in male mating ability and inbreeding depression could potentially lead to the long
74 The selfer population experienced much lower inbreeding depression (delta = 0.05 +/- 0.02 SE) than th
75 ditions, there was a large sex difference in inbreeding depression (delta) and the inbreeding load (L
77 In this way we introduce the concept of "inbreeding depression effect variance," a parameter more
78 levels of inbreeding and reduced fitness via inbreeding depression, even as the population remained d
81 ns and compared mean fitness, heterosis, and inbreeding depression for eight large and eight small po
85 ., 12,000-65,000) will be required to detect inbreeding depression for likely effect sizes, and so st
86 quency of these major mutations, most of the inbreeding depression for male fertility and cumulative
89 population indicate that there is tremendous inbreeding depression for nearly every fitness component
92 e-sterility alleles contribute to 31% of the inbreeding depression for the fraction of viable pollen
94 etween the neutral and selected loci and the inbreeding depression from the selected locus, irrespect
95 s inherent disadvantage are the avoidance of inbreeding depression generated by selfing and the abili
96 cly available computer program titled 'IDG' (Inbreeding Depression Genetics) to execute these procedu
97 pression by: (1) predicting the variation in inbreeding depression given arbitrary initial genetic va
98 nant role of semilethal alleles in embryonic inbreeding depression has implications for the evolution
99 inance was responsible for the observed high inbreeding depression, heterozygote advantage could not
100 If we are to understand the evolution of inbreeding depression (i.e., purging), we need quantitat
101 contribute to variability in the strength of inbreeding depression (ID) observed across adverse envir
105 lower fertility; (ii) offspring suffer from inbreeding depression; (iii) parents have more grandchil
106 gest evidence to date of an HFC being due to inbreeding depression in a natural population lacking a
107 is to provide information on the genetics of inbreeding depression in a primarily outcrossing populat
109 amounts to an approximately 69% increase in inbreeding depression in a stressful vs a benign environ
110 resolve the long-standing paucity of data on inbreeding depression in adult traits and total fitness.
111 and suggest that, to date, the prevalence of inbreeding depression in adult traits may have been unde
113 y, which revealed similar starting levels of inbreeding depression in both breeding systems, but also
115 er, very little is known about the levels of inbreeding depression in dioecious species, obviously be
116 and comparatively complete pedigree detected inbreeding depression in juvenile survival, but not in a
119 s for both the low mean and high variance in inbreeding depression in M. annua, and we discuss the im
121 to be ubiquitous among studies that examine inbreeding depression in multiple environments, and a pr
122 Data are presented on mating systems and inbreeding depression in multiple populations of two ann
123 tially recessive deleterious alleles causing inbreeding depression in natural plant populations.
124 , spatial genetic structure, and sporophytic inbreeding depression in natural populations of a dioico
125 eding provide a powerful tool for evaluating inbreeding depression in natural populations, and sugges
126 study were to: (1) quantify the strength of inbreeding depression in North-American populations of A
127 ous studies have suggested that early-acting inbreeding depression in plants is primarily due to leth
129 his hypothesis by comparing the magnitude of inbreeding depression in self-incompatible and self-comp
130 t tool for mitigating detrimental effects of inbreeding depression in small, inbred populations, but
131 ny genetic disorders in humans and producing inbreeding depression in the majority of sexually reprod
132 y play an important role as a buffer against inbreeding depression in the offspring by alleviating th
134 um effective population size to avoid severe inbreeding depression in the short term is of the order
136 the coexistence of moderate selfing and high inbreeding depression in this strongly protandrous Silen
141 itness component and that almost all of this inbreeding depression is due to mildly deleterious allel
144 Understanding the genetic architecture of inbreeding depression is important in the context of the
146 reveals the important difference between how inbreeding depression is measured experimentally and how
152 th America except in southern Florida, where inbreeding depression led to reproductive failure [3-5].
153 for all life history stages, with cumulative inbreeding depression less than 0.23 in all populations.
154 llowing long-distance dispersal, declines in inbreeding depression may also be facilitated by genetic
155 Therefore, we identify two ways by which inbreeding depression may be underestimated in studies o
156 ation among individuals in the expression of inbreeding depression may reflect lineage-specific diffe
158 Taken together, these findings suggest that inbreeding depression negatively impacts the overall pat
159 ome size of Arabidopsis, and the equilibrium inbreeding depression observed in this highly selfing pl
162 and short-term lowering of fitness owing to inbreeding depression, of which the latter appears the m
165 and improvements in biomedical correlates of inbreeding depression, provide strong evidence that gene
168 non-lethal mutations, reducing the amount of inbreeding depression relative to that expected without
169 t in captivity may decrease the intensity of inbreeding depression, relative to the stressful conditi
171 effects could have several causes, including inbreeding depression, shared incompatibility alleles, o
174 of closely related parents often suffer from inbreeding depression, sometimes resulting in a slower g
175 In line with the prediction of sporophytic inbreeding depression sporophyte size was significantly
177 nding inconvertible evidence of the cause of inbreeding depression still presents a difficult challen
179 its retention is accompanied by substantial inbreeding depression, suggesting that it is caused by m
182 ctions with insects can increase or decrease inbreeding depression (the loss of fitness due to self-f
183 important consequences for phenomena such as inbreeding depression, the evolution of diploidy, and le
184 iation in natural populations, the nature of inbreeding depression, the evolution of sexual reproduct
185 eduction in fitness-related traits known as "inbreeding depression." There is mounting evidence that
186 lternatively, the partial dominance model of inbreeding depression typically applied to polyploids ma
187 ogeny; (iii) differing values of selfing and inbreeding depression using population means vs. matched
189 70-85% using population means; in all cases, inbreeding depression values were high in early and late
191 h theoretical expectations, the magnitude of inbreeding depression was lower in L. bicolor, the more
192 large populations (mean = 7%, SE = 27); and inbreeding depression was lower, although not significan
193 rogeny were grown in a common greenhouse and inbreeding depression was measured in germination, survi
194 udy of Scots pine from Finland, the level of inbreeding depression was much lower in northern than in
196 -incompatibility or to extreme, early acting inbreeding depression, we performed three diallel crosse
197 tive ability of pollen, as well as levels of inbreeding depression, we predict that the early product
199 as the potential to moderate the severity of inbreeding depression, which in turn may favor inbreedin
201 of standing variation for fitness traits is inbreeding depression, with its converse of heterosis or
202 terious mutations, reducing mean fitness and inbreeding depression within populations and increasing
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