Identification of ten chromosome deficiencies of cotton

Endrizzi, J. E.; Ramsay, G.

doi:10.1093/oxfordjournals.jhered.a109309

Cited by 29 publications

(19 citation statements)

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“…These results were confirmed by their following study on QTL mapping for lint percentage and fiber quality traits (micronaire, uniformity, and fiber elongation) using an n 2 mutant derived population (Rong et al 2007). However, all these results were based on their conclusion that both fuzzless loci (N 1 and n 2 ) were on chromosome 12 of the tetraploid cotton genome; but N 1 and n 2 were originally regarded as a pair of homoeologous loci on the long arm of chromosomes 12 and 26 (Endrizzi and Ramsay 1980;Endrizzi et al 1984;Samora et al 1994). Instead of using the single fuzzless locus mutant developed mapping populations (Rong et al 2005(Rong et al , 2007Zhang et al 2005;Guo et al 2006;Wan et al 2007), the common female parent line of the two F 2 populations we developed combined at least two fuzzless loci (N 1 and n 2 , and probably n 3 ) (Turley and Kloth 2002).…”

Section: Discussionmentioning

confidence: 99%

Use of fiber and fuzz mutants to detect QTL for yield components, seed, and fiber traits of upland cotton

Jenkins

et al. 2009

Euphytica

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This research detected QTL or molecular markers associated with yield, fiber, and seed traits within multiple fuzz and fiber loci genetic backgrounds. Two F 2 populations from crosses of MD17, a fuzzless-lintless line containing three fuzzless loci, N 1 , n 2 and a postulated n 3 , with line 181, fuzzlesslinted and with FM966, a fuzzy-linted cultivar, were used. QTL explaining 68.3 (population with FM966) to 87.1% (population with 181) of the phenotypic variation for lint percentage and 62.8% (population with 181) for lint index were detected in the vicinity of BNL3482-138 on chromosome 26. Single marker regression analyses indicated STV79-108, on the long arm of chromosome 12 had significant association with lint percentage (R 2 26.7%), lint index (R 2 30.6%), embryo protein percentage (R 2 15.4%) and micronaire (R 2 20.0%). Two-locus epistatic interactions were also observed. Results from this research will facilitate further understanding the complex mechanisms of yield, fiber, and seed traits of cotton.

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Section: Discussionmentioning

confidence: 99%

Use of fiber and fuzz mutants to detect QTL for yield components, seed, and fiber traits of upland cotton

Jenkins

et al. 2009

Euphytica

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“…1). These relationships becomes more intriguing when considering that N 1 and n 2 may be homoeologous loci on the homeologous chromosome 12 and 26 (Endrizzi and Ramsay 1980;Samora et al 1994). A recent genetic map, however, reports that the n 2 locus was not located on chromosome 26, but on chromosome 12 (Rong et al 2005).…”

Section: Discussionmentioning

confidence: 99%

The inheritance model for the fiberless trait in upland cotton (Gossypium hirsutum L.) line SL1-7-1: variation on a theme

Turley

Kloth

2008

Euphytica

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Segregating populations were developed to evaluate the inheritance of the fiberless seed phenotype of upland cotton (Gossypium hirsutum L.) line SL1-7-1. We report the inheritance of fuzzy, fuzzless and fiberless seed from crosses of SL1-7-1 with wildtype DP5690, Mexican fuzzless seed UA 3-3 (accession 143), Ballard fuzzless seed (accession 243), and MD17. Results from the F 1 , F 2 and F 2:3 progeny derived from the SL1-7-1 X DP5690 indicated that the expression of the fiberless phenotype fit a three loci model with one locus being the dominant fuzzless seed allele N 1 . The other two loci were tested to verify whether they were allelic to either recessive fuzzless seed alleles n 2 or n 3 . Using the segregation ratios of the F 2 progeny derived from the 143 X SL1-7-1 cross and F 2 -derived F 3 families from SL1-7-1 X DP5690 with fuzzy seed (lacked N 1 ), it is proposed that SL1-7-1 lacks the recessive n 2 allele, but contains the n 3 allele in the genotype of SL1-7-1. The third locus was previously not characterized and has been designated as fl 1 (fiberless), therefore, the genotype for the fiberless phenotype of SL1-7-1 is N 1 N 1 fl 1 fl 1 n 3 n 3 . Fiberless lines MD17 X SL1-7-1 were crossed to verify similarities in genotypes between line and the genotype model predictability. Various combinations of the homozygous and heterozygous expression of N 1 , n 2 , n 3 and fl 1 allele produced plants with lower lint percentages.

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“…A genetic study of the MCU5 fiberless line suggested that its fiberless character is controlled by two to four loci (Nadarajan and Rangasamy, 1988), and based on the reported segregation of F 2 progeny, that the MCU5 line has either the n 2 or n 3 locus along with other loci (Turley and Kloth, 2008). It was speculated later that the inhibitor gene could be equivalent to the dominant N 2 gene, since naked seeds have a tufted phenotype (Du et al, 2001). It was speculated later that the inhibitor gene could be equivalent to the dominant N 2 gene, since naked seeds have a tufted phenotype (Du et al, 2001).…”

Section: Fiberless Mutantsmentioning

confidence: 99%

“…The n 2 locus is homeologus to N 1 , and resides on chromosome D12 (chromosome 26) (Endrizzi andRamsay, 1980, Zhu et al, 2018). To prove this, Du et al (2001) made a variety of crosses using different mutant lines. Rather than N 1 or n 2 , Turley and Kloth (2002) proposed a third locus n 3 controlling fuzzless trait when studying the genetic control of the fuzzless trait in cotton lines 143 and 243.…”

Section: Fiberless Mutantsmentioning

confidence: 99%

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Unraveling Cotton Fiber Development Using Fiber Mutants in the Post‐Genomic Era

2018

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Cotton (Gossypium spp.) fibers are unicellular trichomes that differentiate from ovule epidermal cells. Cotton fiber development is divided into four distinct yet overlapping stages: initiation, elongation, secondary cell wall (SCW) biosynthesis, and maturation. There are numerous naturally occurring and man‐made fiber mutants that display aberrant phenotypes ranging from fiberless to extremely short fiber, and to immature fiber. These mutants have provided cotton researchers an excellent model system to study fiber growth and development. During the past two decades, much advancement in the understanding of fiber development has been achieved through comparative analyses of fiber mutants and wild‐type cotton lines using a variety of technologies such as transcriptomic analysis and genetic mapping. The causative genes of five mutations related to fiber initiation, elongation, or SCW assembly have been identified. Lint and fuzz fiber initiations are regulated by MYBMIXTA‐like transcription factors along with many other genes. Cytoskeleton actins play a critical role in fiber elongation. Genes that are involved in biological processes such as transporting osmoticum or loosening cell walls are highly expressed during the elongation stage. Production of large amounts of cellulose at the SCW stage requires a sustainable supply of energy and carbohydrate precursors. Plant hormones affect fiber development. In this paper, we review progress in the elucidation of fiber development mechanisms based on analyzing fiber mutants and summarize genes and mechanisms that are critical to fiber development. We identify research gaps that should be future research priorities and provide a future perspective.

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Identification of ten chromosome deficiencies of cotton

Cited by 29 publications

References 0 publications

Use of fiber and fuzz mutants to detect QTL for yield components, seed, and fiber traits of upland cotton

Use of fiber and fuzz mutants to detect QTL for yield components, seed, and fiber traits of upland cotton

The inheritance model for the fiberless trait in upland cotton (Gossypium hirsutum L.) line SL1-7-1: variation on a theme

Unraveling Cotton Fiber Development Using Fiber Mutants in the Post‐Genomic Era

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