全 文 ：作物学报 ACTA AGRONOMICA SINICA 2010, 36(10): 16571665 http://www.chinacrops.org/zwxb/
ISSN 0496-3490; CODEN TSHPA9 E-mail: xbzw@chinajournal.net.cn

This study was supported by the National Basic Research Program (973 Program) (2010CB126001).
* Corresponding author: Lin Zhong-Xu, E-mail: linzhongxu@mail.hzau.edu.cn; Tel: +86-2787283955
Received(收稿日期): 2010-01-19; Accepted(接受日期): 2010-05-20.
DOI: 10.3724/SP.J.1006.2010.01657
Genetic Dissection of Segregation Distortion in Interspecific BC1 Populations of
Cotton
YU Yu1,2, ZHANG Yan-Xin1, LIN Zhong-Xu1,*, and ZHANG Xian-Long1
1 National Key Laboratory of Crop Genetic Improvement & National Centre of Plant Gene Research / Huazhong Agricultural University, Wuhan
430070, China; 2 Cotton Institute, Xinjiang Academy of Agriculture and Reclamation Science, Shihezi 832000, China
Abstract: Segregation distortion (SD) is the deviation of genetic segregation ratios from their expected Mendelian fashion and is
a common phenomenon found in most genetic mapping studies. In our previously genetic map published, 107 SSR markers
showed SD in the BC1 mapping population [(Emian 22×3-79) × Emian 22]. To verify their segregation in other populations and
to clarify the possible mechanism of SD, 97 co-dominant markers of them were evaluated in another two backcross popula-
tions. The results showed that 61 distorted markers in the mapping population segregated normally in the other backcross
populations, which implied that the cross way is a major factor affecting segregation distortion. Thirty-six markers showed
segregation distortion in at least two populations, which is assumed to be caused by gametic selection. These distorted markers
distributed on 14 chromosomes with more markers in D sub-genome than in A sub-genome. Chr.2, Chr.16, and Chr.18 were the
chromosomes with more distorted markers than others, which implies that there must be segregation distortion loci on these
chromosomes, leading us to identify segregation distortion loci in cotton.
Keywords: Cotton; Simple sequence repeats (SSR); Segregation distortion (SD); Backcross population
棉花种间 BC1群体偏分离的遗传剖析
余 渝 1,2 张艳欣 1 林忠旭 1,* 张献龙 1
1 华中农业大学 / 作物遗传改良国家重点实验室及国家植物基因研究中心, 湖北武汉 430070; 2 新疆农垦科学院棉花所, 新疆石河子
832000
摘 要: 偏分离是指观察到的基因型频率偏离预期的孟德尔频率的遗传分离方式, 在大多数的遗传定位研究中非常
普遍。在之前我们发表的遗传连锁图中, 107个 SSR标记在 BC1作图群体[(Emian 22×3-79) × Emian 22]中表现偏分离。
为阐明这些偏分离标记的遗传机制及其在其它群体中的偏分离情况, 将其中 97个共显性标记在另外两个回交群体中
进行验证。结果表明, 原图谱中的 61 个偏分离标记在另外 2个回交群体中都表现正常分离, 说明杂交方式是导致偏
分离的一个重要因素。36 个偏分离标记至少在两个群体中仍表现偏分离, 偏分离应该是配子选择的结果。偏分离标
记分布于 14条染色体上, 其中 D亚基因组上的分布多于 A亚基因组。偏分离标记在在第 2、第 16和第 18染色体上
分布最多, 暗示在这些染色体上存在偏分离位点, 该结果有助于在棉花中鉴定偏分离位点。
关键词: 海岛棉; 微卫星标记; 偏分离; 回交群体
Segregation distortion (SD) can be defined as a devia-
tion from the expected Mendelian proportion of indi-
viduals in a given genotypic class within a segregation
population. SD was firstly reported in maize by Man-
gelsdof and Jones[1]. Mechanisms of SD have been less
studied in plants before. However, with the de-
velopment of molecular marker and oncoming genetic
maps, numerous examples of SD have been reported in a
large number of linkage maps in plants. Genomic regions
harboring markers with SD have been reported in many
crop species including rice[2-4], maize[5-6], wheat[7-9], bar-
ley[10-12], tomato[13], sugar beet[14], alfalfa[15-16], coffee[17],
pearl millet[18-19], etc.
Cotton (Gossypium spp.) is an important cash crop and
the second largest source of textile fiber and edible oil
throughout the world. Great interest has been paid to
cotton genetics and breeding because of its obvious im-
portance. In the past fifteen years, a number of molecular
linkage maps including interspecific maps[20-25] and in-
traspecific maps[26-29] were constructed and applied to
analyze economic traits, e.g. fiber yield and fiber qua-
lity[22,28,30-31]. Among these mapping populations, inter-
1658 作 物 学 报 第 36卷

specific populations between upland cotton and sea-
island cotton are most widely used because of the high
polymorphic ratio of molecular markers in such popula-
tions. During the development of molecular maps, SD
has been frequently detected in cotton mapping popula-
tions. Lacape et al.[21] reported that 8.5% of the markers
showed SD in their interspecific BC1 population. In the
BC1 genetic linkage map, 105 loci (12.3%) showed SD
and two distorted intervals were found on Chr.7 and
Chr.16[24]. In our previously published interspecific ge-
netic map, 18.0% of the markers showed SD[32]. In our
recently published interspecific linkage map[25], signifi-
cant SD was observed on 107 loci (11.7%).
The objective of this study was to figure out the rea-
sons of SD in this interspecific BC1 population [25] using
two other backcross populations based on the same F1
and parents of this population. The experimental plan
was designed to study the influence of gamete selection
on SD.
1 Materials and Methods
1.1 Plant materials and population development
The development of backcross populations is listed in
Fig. 1. G. hirsutum L. cv. “Emian 22” as female and G.
barbadense L. acc. “3-79” as male were crossed to pro-
duce F1. The population 1 (Pop 1) including 141 indi-
viduals was denoted as the interspecific BC1 population
[(Emian 22 × 3-79) × Emian 22][25]. For the population 2
(Pop 2), “Emian 22” was used as female and the F1 as
male to develop the interspecific BC1 population [Emian
22× (Emian 22 × 3-79)]. For the population 3 (Pop 3),
the F1 was used as female and the “3-79” as male to de-
velop the interspecific BC1 population [(Emian 22 ×3-79)
× 3-79]. One hundred and fifteen individuals from Pop 2
and 116 individuals from Pop 3 were randomly selected.
All materials were planted in the fields at Huazhong
Agricultural University.

Fig. 1 Developed backcross populations for SD analysis

1.2 DNA isolation
Total genomic DNA was isolated from the young leaf
tissue of the individual plants according to Paterson et
al.[33].
1.3 SSR analysis and marker coding
Ninety-seven segregation distorted co-dominant SSR
markers were selected from Pop 1 and were analyzed in
Pop 2 and Pop 3[25]. Polymerase chain reactions (PCR),
electrophoresis and silver staining were conducted based
on the protocols of Lin et al.[32].
1.4 Segregation ratio test and chromosome as-
signment of distorted loci
A chi-square test (P < 0.05) was performed to deter-
mine if the genotypic frequencies at each locus deviated
from the expected 1:1 segregation ratio. The segregation
classes of each locus were defined according to the ob-
served genotype number compared to the expected num-
ber at the significant level (P < 0.05). The chromosome
locations of distorted loci were based on the linkage map
of Zhang et al.[25]
2 Results
2.1 Characteristics of segregation distorted mark-
ers (SDMs)
Only ninety-seven co-dominant markers were ana-
lyzed in Pop 2 and Pop 3, because dominant markers in
Pop 1 did not segregate in Pop 3. There were sixty-one
distorted markers in Pop 1 that segregated in a Mendelian
fashion both in Pop 2 and Pop 3, among which twenty
markers had excess “Emian 22” homozygotes and
forty-one had deficient “Emian 22” homozygotes.
Thirty-six markers (59%) showed SD at the significant
level of P<0.05; five, eleven, three, two and four at the
significant level of P<0.01, P<0.005, P<0.001, P<0.0005,
and P<0.0001, respectively (Table 1).
Seventeen SDMs showed segregation distorted both in
Pop 1 and Pop 2, but not in Pop 3. The sixteen markers
had deficient “Emian 22” homogygotes and excess het-
erozygotes in Pop 1; however, only nine of them had the
same segregation class and the others oppositely segre-
gated in Pop 2. Only BNL3436 had excess “Emian 22”
homogygotes and deficient heterozygotes in Pop 1, but it
oppositely segregated in Pop 2. Nine SDMs showed
more severe distortion in Pop 2 than in Pop 1, four
showed similar distortion in both populations, and four
showed more severe distortion in Pop 1 than in Pop 2
(Table 2).
Fifteen SDMs showed segregation distortion both in
Pop 1 and Pop 3, but not in Pop 2. There were twelve
markers having excess heterozygotes and three having
deficient heterozygotes; in Pop 3, only seven ones having
excess heterozygotes and eight having deficient het-
erozygotes. Five markers had excess heterozygotes in
both populations, and one marker had deficient het-
erozygotes in these two populations. Six SDMs showed
more severe distortion in Pop 3 than in Pop 1, four
showed similar distortion in both populations, and five
showed more severe distortion in Pop 1 than in Pop 3
(Table 3).
第 10期 YU Yu et al.: Genetic Dissection of Segregation Distortion in Interspecific BC1 Populations of Cotton 1659


Table 1 SDMs only in Pop 1 but not in Pop 2 and Pop 3
Segregation classes Segregation classes
Marker
Emian 22 homozygote Heterozygote
Marker
Emian 22 homozygote Heterozygote
BNL645****** Excess Deficient BNL3287**** Deficient Excess
BNL846* Excess Deficient BNL3793* Deficient Excess
BNL2609* Excess Deficient BNL3971* Deficient Excess
BNL2646****** Excess Deficient BNL4079** Deficient Excess
BNL3875* Excess Deficient CIR020a*** Deficient Excess
BNL4015* Excess Deficient CIR107*** Deficient Excess
CML45* Excess Deficient CIR373* Deficient Excess
DPL442* Excess Deficient CIR376* Deficient Excess
DPL681**** Excess Deficient CIR401b** Deficient Excess
MGHEMS66* Excess Deficient CML63** Deficient Excess
JESPR63***** Excess Deficient DPL079* Deficient Excess
MUSB1112b* Excess Deficient DPL168**** Deficient Excess
MUSB1242* Excess Deficient DPL385**** Deficient Excess
NAU2156****** Excess Deficient DPL511**** Deficient Excess
NAU2302* Excess Deficient DPL519* Deficient Excess
STV120* Excess Deficient DPL674* Deficient Excess
TMB0086* Excess Deficient DPL901a*** Deficient Excess
TMB0635* Excess Deficient MGHEMS22* Deficient Excess
TMB1919*** Excess Deficient HAU042b****** Deficient Excess
TMHE18* Excess Deficient JESPR297*** Deficient Excess
BNL193* Deficient Excess JESPR304* Deficient Excess
BNL1040* Deficient Excess JESPR305* Deficient Excess
BNL1410* Deficient Excess MUSB0953a* Deficient Excess
BNL1521* Deficient Excess NAU2439* Deficient Excess
BNL1721* Deficient Excess STV025* Deficient Excess
BNL2544* Deficient Excess TMB1820***** Deficient Excess
BNL2734a*** Deficient Excess TMB2762** Deficient Excess
BNL2734b** Deficient Excess TMB2944* Deficient Excess
BNL2766*** Deficient Excess TMHB04b* Deficient Excess
BNL3008*** Deficient Excess TMHB09*** Deficient Excess
BNL3280* Deficient Excess
*P<0.05, **P<0.01, ***P<0.005, ****P<0.001, *****P<0.0005, and ******P<0.0001.

Table 2 SDMs both in Pop 1 and Pop 2 but not in Pop 3
Segregation classes in Pop 1 Segregation classes in Pop 2
Marker
Emian 22 homozygote Heterozygote
Marker
Emian 22 homozygote Heterozygote
BNL3871* Deficient Excess BNL3871**** Excess Deficient
CML60* Deficient Excess CML60****** Excess Deficient
DPL216* Deficient Excess DPL216* Excess Deficient
DPL652* Deficient Excess DPL652**** Excess Deficient
HAU033* Deficient Excess HAU033*** Excess Deficient
MUSS073*** Deficient Excess MUSS073*** Excess Deficient
TMB0514* Deficient Excess TMB0514** Excess Deficient
BNL580**** Deficient Excess BNL580* Deficient Excess
BNL1231* Deficient Excess BNL1231*** Deficient Excess
BNL1604*** Deficient Excess BNL1604**** Deficient Excess
BNL2895***** Deficient Excess BNL2895****** Deficient Excess
BNL3371***** Deficient Excess BNL3371***** Deficient Excess
DPL342***** Deficient Excess DPL342* Deficient Excess
MUSB0685a****** Deficient Excess MUSB0685a****** Deficient Excess
MUSS250* Deficient Excess MUSS250*** Deficient Excess
TMB2553****** Deficient Excess TMB2553***** Deficient Excess
BNL3436****** Excess Deficient BNL3436** Deficient Excess
*P<0.05, **P<0.01, ***P<0.005, ****P<0.001, *****P<0.0005, and ******P<0.0001.
1660 作 物 学 报 第 36卷

Table 3 SDMs both in Pop 1 and Pop 3 but not in Pop 2
Segregation classes in Pop 1 Segregation classes in Pop 3
Marker
Emian 22 homozygote Heterozygote
Marker
3-79 homozygote Heterozygote
BNL569a* Deficient Excess BNL569a*** Deficient Excess
BNL1079** Deficient Excess BNL1079* Excess Deficient
BNL2582* Deficient Excess BNL2582* Deficient Excess
BNL2651* Deficient Excess BNL2651****** Deficient Excess
BNL3033* Deficient Excess BNL3033**** Excess Deficient
BNL3479* Deficient Excess BNL3479* Excess Deficient
BNL3558** Deficient Excess BNL3558* Excess Deficient
BNL3790** Deficient Excess BNL3790* Deficient Excess
DPL049* Deficient Excess DPL049***** Excess Deficient
MUSS172* Deficient Excess MUSS172****** Excess Deficient
PGCT116****** Deficient Excess PGCT116** Deficient Excess
TMB0071****** Deficient Excess TMB0071****** Excess Deficient
BNL1080** Excess Deficient BNL1080**** Deficient Excess
CIR381***** Excess Deficient CIR381**** Deficient Excess
NAU2381* Excess Deficient NAU2381* Excess Deficient
*P<0.05, **P<0.01, ***P<0.005, ****P<0.001, *****P<0.0005, and ******P<0.0001.

Four markers showed SD in all three populations.
BNL2652 had excess heterozygotes in Pop 1 and Pop 2,
but deficient heterozygotes in Pop 3; it showed more
severe distortion in Pop 2 than in Pop 1 and Pop 3.
BNL3034 had deficient heterozygotes in Pop 1 and Pop 2,
but excess heterozygotes in Pop 3; it also showed more
severe distortion in Pop 2 than in Pop 1 and Pop 3.
JESPR237 and MUSS1402 had excess heterozygotes in
three populations; JESPR237 showed more severe distor-
tion in Pop 1 than in Pop 2 and Pop 3, but MUSS1402
showed the similar distortion in three populations (Table
4).
2.2 SDMs distribution on Chromosomes of dif-
ferent backcross populations
For the ninety-seven SDMs in Pop 1, most of them
clustered on special regions of limited cotton chromo-
somes; however, some of them sparsely distributed on
different chromosomes. It was impossible to construct
linkage groups in Pop 2 and Pop 3 because SDMs were
analyzed only in Pop 1. Therefore, in this section, the
chromosome location of SDMs in Pop 2 and Pop 3 were
based on the linkage map constructed in Pop 1.
A total of thirty-six SDMs in Pop 1 showed segrega-
tion distortion in Pop 2 or Pop 3. Among them, thirty-five
markers were located on fourteen chromosomes con-
structed by Pop 1; one marker (BNL3033) was not lo-
cated in this linkage map. Fifteen SDMs distributed on
six chromosomes of the A sub-genome, and twenty-one
SDMs on eight chromosomes of the D sub-genome. Five,
four, four and eight SDMs distributed on Chr.2, Chr.7,
Chr.16, and Chr.18, respectively; the left SDMs sparsely
distributed on the other eleven chromosomes (Fig. 2).

Table 4 SDMs in three populations
Population Marker Emian 22 homozygote Heterozygote
BNL2652* Deficient Excess
BNL3034* Excess Deficient
JESPR237*** Deficient Excess
Segregation classes in Pop 1
MUSS140****** Deficient Excess
Emian 22 homozygote
BNL2652*** Deficient Excess
BNL3034****** Excess Deficient
JESPR237* Deficient Excess
Segregation classes in Pop 2
MUSS140****** Deficient Excess
3-79 homozygote
BNL2652* Excess Deficient
BNL3034* Deficient Excess
JESPR237** Deficient Excess
Segregation classes in Pop 3
MUSS140****** Deficient Excess
*P<0.05, **P<0.01, ***P<0.005, ****P<0.001, *****P<0.0005, and ******P<0.0001.
第 10期 YU Yu et al.: Genetic Dissection of Segregation Distortion in Interspecific BC1 Populations of Cotton 1661





1662 作 物 学 报 第 36卷



Fig. 2 SDMs distribution of on chromosome of different backcross populations
SDMs both in Pop 1 and Pop 2 in bold, SDMs both faced in Pop 1 and Pop 3 are underlined, SDMs in all three populations are boldfaced and
underlined.
第 10期 YU Yu et al.: Genetic Dissection of Segregation Distortion in Interspecific BC1 Populations of Cotton 1663


SDMs both in Pop 1 and Pop 2 distributed on Chr.2,
Chr.7, Chr.11, Chr.14, Chr.16, Chr.17, Chr.18, Chr.21,
Chr.24, and Chr.25; Chr.2, Chr.7, Chr.16, and Chr.18
harbored more SDMs. Eight SDMs located on three
chromosomes of A sub-genome and thirteen on seven
chromosomes of D sub-genome. SDMs both in Pop 1 and
Pop 3 distributed on Chr.2, Chr.3, Chr.9, Chr.13, Chr.14,
Chr.16, Chr.18, Chr.24, and Chr.26; Chr.18 had the most
SDMs with six ones on it. Seven SDMs located on four
chromosomes of A sub-genome and eleven on five
chromosomes of D sub-genome (Fig. 2).
3 Discussion
Segregation distortion is an often encountered problem
in mapping studies, and it may influence the mapping
accuracy. In cotton, SD has been found both in inter-
specific and intraspecific populations[21,24-25,27-29]. How-
ever, these SDMs were only analyzed in single popula-
tion, and the genetic basis of segregation distortion is still
poorly understood. In our previous work, an interspecific
genetic linkage map of tetraploid cotton based on BC1
population was constructed, and 107 loci were found to
be distorted in segregation[25]. Backcross population was
a major mapping population in cotton mapping[21,24-25].
Although backcross population can be generated in dif-
ferent ways, only one kind of backcross population was
involved in cotton, i.e. [(G. hirsutum × G. barbadense) ×
G. hirsutum]. In order to show the SD in other backcross
populations and to discuss the possible causes of SD, the
SDMs in the BC1 map [25] were tested in another two
backcross populations.
“Emian 22” is an upland cotton cultivar which was
approved in 1998 in Hubei province, and was once
widely cultivated and used as parent for hybrid produc-
tion in Hubei province. Sea-island cotton accession
“3-79” is the genetic and cytogenetic standard line for G.
barbadense, which is adopted worldwide in cotton ge-
netics. Upland cotton and sea-island cotton are sexually
compatible[34]. Their hybrid is vigorous and widely ap-
plied to generate interspecific mapping populations[20-25],
so the interspecific F1 is an ideal material for analyzing
gamete selection on SD in cotton.
In the present study, among the one hundred and seven
SDMs in the backcross population [25] (Pop 1), only
ninety-seven co-dominant ones were analyzed in Pop 2
and Pop 3. The results showed that only twenty-one and
nineteen ones were SD in Pop 2 and Pop 3, respectively.
In plant genetics and breeding, the cross way of Pop 1 is
the most frequently adopted one. However, there is more
segregation distortion in this kind of population based on
this study. On the contrary, there were only few SD in
Pop 2 and Pop 3. In the development of backcross popu-
lation, the parent is usually local cultivar when crossed
with the F1 so that it is more acclimatized to local eco-
logical condition. Based on these considerations, the
cross way of Pop 2 is more suitable for population con-
struction.
Segregation distortion is influenced by many factors,
for example, mapping population[9,35], pollen tube com-
petition[1], preferential fertilization of particular gametic
genotypes[36-37], gametic and zygotic selections[38-39]. SD
caused by gametophyte selection has been well docu-
mented[2-5,39-40]. In the present study, sixty-one SDMs in
Pop 1 did not show segregation distorted in Pop 2 and
Pop 3, which should be derived from the different cross
ways. Seventeen SDMs showed segregation distorted
both in Pop 1 and Pop 2 but not in Pop 3. These markers
had the same female parent in Pop 1 and Pop 3, and the
expected heterozygotes in Pop 3 indicated that no selec-
tion for the female gamete of “Emian 22”. Eight SDMs
had opposite gamete ratio between homozygotes and
heterozygotes in Pop 1 and Pop 2, but expected gamete
ratio in Pop 3. So the SD of these markers may be caused
by the selection of the male gamete of “Emian 22” for the
female gamete, which could be further confirmed in the
[3-79 × (Emian 22 × 3-79)] population. The other nine
SDMs had the same gamete ratio in the two populations
with deficient homozygotes, which indicated that the SD
of these markers resulted from inferior combination of
“Emian 22” homozygotes.
Fifteen SDMs showed segregation distortion both in
Pop 1 and Pop 3, but not in Pop 2. These markers had the
same female parent, but different male parent, so the SD
was caused by male gamete selection on female gametes.
Five SDMs (BNL569a, BNL2582, BNL2651, BNL3790,
and PGCT116) had excess heterozygotes in both popula-
tions, but had expected heterozygotes in Pop 2, which
indicated that the SD was caused by inferior combination
of homozygotes. NAU238 had deficient heterozygotes in
both populations, which implied the SD was caused by
preferential combination of homozygotes. The other
eight SDMs had opposite gamete ratio in Pop 1 and Pop
3, which may be caused by different selection of male
gamete. Four markers showed SD in all three populations.
BNL2652 and BNL3034 had different gamete ratio in
three populations, which may be caused by different se-
lection of female or male gamete. JESPR237 and
MUSS1402 had excess heterozygotes in three popula-
tions, which resulted from preferential fertilization of
exotic gametes.
The SDMs in Pop 1 showed eleven segregation distor-
tion regions with two in A sub-genome and nine in D
sub-genome[25]. In this study, some SD disappeared in
Pop 2 and Pop 3; however, common SDMs were found
between the three populations. Although SDMs distrib-
uted on similar number of chromosomes of the A and D
sub-genome, more SDMs distributed on the chromo-
somes of the D sub-genome. What’s more, SDMs un-
evenly distributed on the fourteen chromosomes with
more SDMs on Chr.2, Chr.16, and Chr.18; these chro-
1664 作 物 学 报 第 36卷

mosomes have been proved to harbor more SDMs by
other maps[20-24]. We presumed that there must be segre-
gation distortion loci on the three chromosomes. Faris et
al. [39] and Kumar et al.[40] mapped segregation distortion
loci using reciprocal backcross populations, which could
be very helpful for us to identify segregation distortion
loci in cotton.
4 Conclusion
The cross way and gametic selection are the major
factors affecting segregation distortion in cotton. Dis-
torted markers mainly distributed on Chr.2, Chr.16, and
Chr.18, which imply that there must be segregation dis-
tortion loci on these chromosomes.
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