GENETIC SUPPRESSION AND PHENOTYPIC MASKING OF A MYXOCOCCUS-XANTHUS FRZF(-) DEFECT

GENETIC SUPPRESSION AND PHENOTYPIC MASKING OF A MYXOCOCCUS-XANTHUS FRZF(-) DEFECT
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DOI:
10.1111/j.1365-2958.1995.tb02262.x
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发表时间:
1995-02-01
影响因子:
3.6
通讯作者:
HARTZELL, PL
HARTZELL, PL
中科院分区:
生物学2区
文献类型:
--
作者:
KASHEFI, K;HARTZELL, PL

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转座子Tn5-lac的插入Omega 4519与黄粘球菌在营养生长和发育过程中表达的启动子产生lacZ融合,对Omega 4519与黄粘球菌DNA连接的序列分析表明,该插入位于鼠伤寒沙门氏菌cheR的同源物frzF中。当frzF(-)(或frzCD(-))细胞在适度密度下缺乏营养时,它们聚集形成放射状模式,产生不到1%的野生型孢子补体。在较高的密度下,frzF::Omega 4519细胞形成卷曲的聚集体,产生80-90%的野生型孢子补体。相反,当frzF(-)(或fizCD(-))和sglA1突变的细胞在低或高细胞密度下发育时,它们产生卷曲的聚集体,含有接近野生型的耐热孢子补体。除了抑制子体形态发生的密度依赖性,SglA1突变还抑制由两个不同的frzF(-)突变和一个frzCD(-)突变引起的产孢缺陷,相反,另一个S动力基因sglG1的突变不抑制frz(-)突变,因此,sgl(-)突变对frz(-)突变的抑制是等位基因特异性的,取决于sgl等位基因,而不是frz等位基因,因为frz(-)突变的表型是在(抑制)SglA1遗传背景下确定的。FRZ基因可能在发育过程中发挥比最初认识到的更重要的作用。
An insertion of transposon Tn5-lac, Omega 4519, generates a lacZ fusion with a Myxococcus xanthus promoter expressed during both vegetative growth and development, Sequence analysis of the junction of Omega 4519 with M. xanthus DNA shows that the insertion is in frzF, a homologue of cheR from Salmonella typhimurium. When frzF(-) (or frzCD(-))cells are starved for nutrients at modest densities, they aggregate to form a radial pattern and produce fewer than 1% of the wildtype complement of spores. At higher densities, frzF::Omega 4519 cells form 'frizzy' aggregates and produce 80-90% of the wild-type complement of spores, In contrast, when cells with both a frzF(-) (or fizCD(-)) and an sglA1 mutation are allowed to develop at either low or high cell densities, they produce frizzy aggregates containing a near wild-type complement of heat-resistant spores, In addition to suppressing the density dependence of fruiting-body morphogenesis, the SglA1 mutation also suppresses the sporulation defect caused by two different frzF(-) mutations and a frzCD(-) mutation, In contrast, a mutation in a different S motility gene, sglG1, does not suppress the frz(-) mutations, Thus, the suppression of frz(-) mutations by sgl(-) mutations is allele-specific, and depends on the sgl allele, but not the frz allele, Because the phenotypes of frz(-) mutations have been determined in a (suppressing) sglA1 genetic background, the frz genes may play more central roles in development than initially recognized.