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Glycinebetaine deficiency in maize.

Yang, Wen-Ju.

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Glycinebetaine deficiency in maize.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Glycinebetaine deficiency in maize./
作者:	Yang, Wen-Ju.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 1994,
面頁冊數:	94 p.
附註:	Source: Dissertation Abstracts International, Volume: 55-12, Section: B, page: 5155.
Contained By:	Dissertation Abstracts International55-12B.
標題:	Plant biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9513093

Glycinebetaine deficiency in maize.
Yang, Wen-Ju.

Glycinebetaine deficiency in maize. - Ann Arbor : ProQuest Dissertations & Theses, 1994 - 94 p.

Source: Dissertation Abstracts International, Volume: 55-12, Section: B, page: 5155.

Thesis (Ph.D.)--Purdue University, 1994.

Glycinebetaine is thought to be an osmoprotectant in higher plants, as in bacteria. Evidence in vitro has been reported that glycinebetaine protects enzymes, membrane structure, and photosynthetic systems against environmental stresses such as heat and salt. However, the function of glycinebetaine in vivo in higher plants is not yet clear. To address the importance of glycinebetaine in higher plants, we have characterized single gene mutants of maize which are defective in glycinebetaine accumulation. Genetic and metabolic studies of glycinebetaine accumulation in maize (Zea mays L.) indicate that recessive alleles of a single locus are responsible for the phenotype of glycinebetaine deficiency and that the lesion is at the choline $\to$ betaine aldehyde step in the biosynthetic pathway. Complementation tests among 20 glycinebetaine-deficient parents suggest that all the glycinebetaine-deficient inbreds and selections tested share a common deficiency gene. Analyses of glycinebetaine levels of reciprocal hybrids made between glycinebetaine-containing and -deficient parents also suggested that maternal effects are negligible. In order to determine the chromosomal location of the gene that confers glycinebetaine accumulation, 48 recombinant inbreds derived from inbreds T232 and CM37 were analyzed (where T232 is glycinebetaine-containing, and CM37 is glycinebetaine-deficient). The locus determining glycinebetaine accumulation (designated bet1) was mapped to the centromere region of chromosome 3. Because CM37 accumulates an alternative betaine (nicotinic acid betaine, trigonelline) whereas T232 lacks this compound, it was also possible to map a second locus (designated trg1) determining trigonelline accumulation to the long arm of chromosome 4. Consistent with the chromosome 3 centromere region location of bet1, analyses of progeny from crosses between glycinebetaine-deficient lines and a glycinebetaine-containing line carrying the vp1 allele, strongly suggest that bet1 and vp1 are linked. A series of near-isogenic F8 pairs of glycinebetaine-containing and -deficient lines were developed. These were used to identify random amplified polymorphic DNA markers which are linked to bet1 and to test whether glycinebetaine accumulation influences salt tolerance in maize. F8 glycinebetaine-containing lines maintain a statistically significantly higher leaf relative water content than glycinebetaine-deficient sister-lines under saline (150 mM NaCl) conditions.Subjects--Topical Terms:

3186449
Plant biology.

Glycinebetaine deficiency in maize.
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520 $a Glycinebetaine is thought to be an osmoprotectant in higher plants, as in bacteria. Evidence in vitro has been reported that glycinebetaine protects enzymes, membrane structure, and photosynthetic systems against environmental stresses such as heat and salt. However, the function of glycinebetaine in vivo in higher plants is not yet clear. To address the importance of glycinebetaine in higher plants, we have characterized single gene mutants of maize which are defective in glycinebetaine accumulation. Genetic and metabolic studies of glycinebetaine accumulation in maize (Zea mays L.) indicate that recessive alleles of a single locus are responsible for the phenotype of glycinebetaine deficiency and that the lesion is at the choline $\to$ betaine aldehyde step in the biosynthetic pathway. Complementation tests among 20 glycinebetaine-deficient parents suggest that all the glycinebetaine-deficient inbreds and selections tested share a common deficiency gene. Analyses of glycinebetaine levels of reciprocal hybrids made between glycinebetaine-containing and -deficient parents also suggested that maternal effects are negligible. In order to determine the chromosomal location of the gene that confers glycinebetaine accumulation, 48 recombinant inbreds derived from inbreds T232 and CM37 were analyzed (where T232 is glycinebetaine-containing, and CM37 is glycinebetaine-deficient). The locus determining glycinebetaine accumulation (designated bet1) was mapped to the centromere region of chromosome 3. Because CM37 accumulates an alternative betaine (nicotinic acid betaine, trigonelline) whereas T232 lacks this compound, it was also possible to map a second locus (designated trg1) determining trigonelline accumulation to the long arm of chromosome 4. Consistent with the chromosome 3 centromere region location of bet1, analyses of progeny from crosses between glycinebetaine-deficient lines and a glycinebetaine-containing line carrying the vp1 allele, strongly suggest that bet1 and vp1 are linked. A series of near-isogenic F8 pairs of glycinebetaine-containing and -deficient lines were developed. These were used to identify random amplified polymorphic DNA markers which are linked to bet1 and to test whether glycinebetaine accumulation influences salt tolerance in maize. F8 glycinebetaine-containing lines maintain a statistically significantly higher leaf relative water content than glycinebetaine-deficient sister-lines under saline (150 mM NaCl) conditions.
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