CONTROL OF CELL TYPE AND GAMETOGENESIS
CONTROL OF CELL TYPE AND GAMETOGENESIS
批准号:
3269864
负责人:
JAMES E HABER
金额:
$23.06万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1976
资助国家:
美国
项目状态:
已结题
起止时间:
1976-01-01 至 1991-06-30
关键词:
Saccharomyces alleles cell cycle cell differentiation cell transformation cell type cytogenetics endonuclease fungal genetics gene complementation gene conversion gene expression gene mutation genetic manipulation genetic mapping genetic markers genetic recombination meiosis messenger RNA microscopy molecular cloning molecular genetics mutagens nucleic acid sequence radiotracer ribosomal RNA sporogenesis temperature sensitive mutant
中文摘要
酿酒酵母的交配型(Mai)基因是
细胞类型、细胞的遗传和生理控制的复杂网络
世系和分化。MAT基因本身的表达
包括通过从沉默的拷贝或供体转座来激活它们,
MAT轨迹的轨迹,其中表示a或Alpha信息。
我们提出的工作旨在通过以下方式理解这一机制
哪些MAT基因是易位的。MAT基因的同源转换是
一种替换/重组事件,其中α序列的拷贝
AT HML或HMR用来代替MAT的信息。这个基因
转换过程是由特定位点的内切酶启动的,但
链转移的分子机制尚不清楚。一
这个项目的主要目标是定义发生的分子事件
在这个换位过程中,识别和表征
反应的中间产物,并定义MAT和MAT上的DNA序列
供体基因是这一过程所必需的。在这方面,该项目
还试图确定MAT基因的切换在哪些方面是相似的
其他有丝分裂重组事件。这个项目的第二个主要目标
是了解MAT基因是如何与供体基因相互作用的。一点儿
是关于如何将远距离序列组合在一起的
高效地参与重组活动。当Mata单元格
开关,它们优先与供体HML相互作用,在左臂
相同的染色体,而MATAlpha细胞选择性地与HMR配对。脱氧核糖核酸
将表征影响这种配对的与MAT相邻的序列,
影响正常捐献者偏好的突变也是如此。
细胞进行减数分裂的能力取决于是否存在
MATA和MATAlpha等位基因和生理信号。实验是
还建议对22个基因中的一大类突变进行表征
当细胞缺乏氨基酸时影响正常的G1期细胞周期停滞
或生长到静止阶段(因此不能产孢子)。
初步实验表明,这些突变会影响一种
影响蛋白质合成、氨基酸生物合成和蛋白质合成的基因网络
细胞周期停滞。
英文摘要
The mating type (MAI) genes of Saccharomyces cerevisiae are part of a
complex network of genetic and physiological controls of cell type, cell
lineage, and differentiation. The expression of the MAT genes themselves
involves their activation by transposition from a silent copy, or donor,
locus to the MAT locus, where either a or Alpha information is expressed.
The work that we have proposed is designed to understand the mechanism by
which MAT genes are transposed. The homothallic switching of MAT genes is
a substitution/recombination event in which a copy of a of Alpha sequences
at HML or HMR is used to replace the information at MAT. This gene
conversion process is initiated by a site-specific endonuclease, but the
molecular mechanism by which strands are transferred is not known. One
major goal of this project is to define the molecular events occurring
during this transposition process, to identify and characterize
intermediates of the reaction and to define what DNA sequences at MAT and
the donor loci are required for this process. In this regard, the project
also seeks to determine in what ways the switching of MAT genes is similar
to other mitotic recombination events. A second major goal of this project
is to understand how the MAT locus interacts with the donor loci. Little
is understood about the ways that distant sequences can be brought together
efficiently to participate in a recombination event. When MATa cells
switch, they preferentially interact with the donor HML, on the left arm of
the same chromosome, while MATAlpha cells selectively pair with HMR. DNA
sequences adjacent to MAT that affect this pairing will be characterized,
as will mutations that affect the normal donor preference.
The ability of cells to undergo meiosis depends both on the presence of
MATa and MATAlpha alleles and on physiological signals. Experiments are
also proposed to characterize a large class of mutations in 22 genes that
affect normal G1 cell cycle arrest when cells are starved for amino acids
or grown to stationary phase (and are thus unable to sporulate).
Preliminary experiments have suggested that these mutations affect a
network of genes that affect protein synthesis, amino acid biosynthesis and
cell cycle arrest.
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DNA damage response and repair of a broken chromosome
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批准号:10622121
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项目类别:
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资助金额:$97.34万
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财政年份:2018
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负责人:JAMES E HABER
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依托单位:
DNA damage response and repair of a broken chromosome
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批准号:10403563
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项目类别:
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资助金额:$94.5万
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财政年份:2018
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负责人:JAMES E HABER
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依托单位:
DNA damage response and repair of a broken chromosome
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批准号:10166868
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项目类别:
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资助金额:$94.5万
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财政年份:2018
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负责人:JAMES E HABER
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依托单位:
DNA damage response and repair of a broken chromosome
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批准号:10387373
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项目类别:
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资助金额:$17.16万
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财政年份:2018
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负责人:JAMES E HABER
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依托单位:
Mutations Arising During DNA Repair
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批准号:8666255
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项目类别:
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资助金额:$190.87万
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财政年份:2014
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负责人:JAMES E HABER
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依托单位:
Mutations Arising During DNA Repair
-
批准号:9059116
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项目类别:
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资助金额:$167.15万
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财政年份:2014
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负责人:JAMES E HABER
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依托单位:
Recombination Mechanisms in Yeast Cell Differentiation
-
批准号:7986554
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项目类别:
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资助金额:$6.18万
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财政年份:2009
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负责人:JAMES E HABER
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依托单位:
Analysis of Break-Induced Replication
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批准号:7477751
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项目类别:
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资助金额:$23.67万
-
财政年份:2006
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负责人:JAMES E HABER
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依托单位:
Analysis of Break-Induced Replication
-
批准号:8514629
-
项目类别:
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资助金额:$28.41万
-
财政年份:2006
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负责人:JAMES E HABER
-
依托单位:
Analysis of Break-Induced Replication
-
批准号:7141410
-
项目类别:
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资助金额:$24.22万
-
财政年份:2006
-
负责人:JAMES E HABER
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依托单位:
Analysis of Break-Induced Replication
-
批准号:7261369
-
项目类别:
-
资助金额:$23.67万
-
财政年份:2006
-
负责人:JAMES E HABER
-
依托单位:
Analysis of Break-Induced Replication
-
批准号:9115180
-
项目类别:
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资助金额:$31.15万
-
财政年份:2006
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负责人:JAMES E HABER
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依托单位:
Analysis of Break-Induced Replication
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批准号:9315161
-
项目类别:
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资助金额:$31.15万
-
财政年份:2006
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负责人:JAMES E HABER
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依托单位:
Analysis of Break-Induced Replication
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批准号:8755011
-
项目类别:
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资助金额:$30.82万
-
财政年份:2006
-
负责人:JAMES E HABER
-
依托单位:
Analysis of Break-Induced Replication
-
批准号:7666735
-
项目类别:
-
资助金额:$23.67万
-
财政年份:2006
-
负责人:JAMES E HABER
-
依托单位:
Analysis of Break-Induced Replication
-
批准号:8116410
-
项目类别:
-
资助金额:$29.45万
-
财政年份:2006
-
负责人:JAMES E HABER
-
依托单位:
Analysis of Break-Induced Replication
-
批准号:8304961
-
项目类别:
-
资助金额:$29.38万
-
财政年份:2006
-
负责人:JAMES E HABER
-
依托单位:
Analysis of Break-Induced Replication
-
批准号:7984563
-
项目类别:
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资助金额:$31.97万
-
财政年份:2006
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负责人:JAMES E HABER
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依托单位:
Arrest, Recovery, and Adaptation from DNA Damage
-
批准号:8576229
-
项目类别:
-
资助金额:$33.21万
-
财政年份:2001
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负责人:JAMES E HABER
-
依托单位:
Arrest, Recovery, and Adaptation from DNA Damage
-
批准号:8725176
-
项目类别:
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资助金额:$33.31万
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财政年份:2001
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负责人:JAMES E HABER
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依托单位:
海外基金