Three new classes of mutations in the Caenorhabditis elegans muscle gene sup-9.
نویسندگان
چکیده
We are studying five interacting genes involved in the regulation or coordination of muscle contraction in Caenorhabditis elegans. A distinctive "rubber-band" muscle-defective phenotype was previously shown to result from rare altered-function mutations in either of two of these genes, unc-93 and sup-10. null mutations in sup-9, sup-10, sup-18 or unc-93 act as essentially recessive suppressors of these rubber-band mutations. In this work, we identify three new classes of sup-9 alleles: altered-function rubber-band, partial loss-of-function and dominant-suppressor. The existence of rubber-band mutations in sup-9, sup-10 and unc-93 and the suppression of these mutations by null mutations in any of these three genes suggest that these proteins are required at the same step in muscle contraction. Moreover, allele-specific interactions shown by the partial loss-of-function mutations indicate that the products of these interacting genes may physically contact each other in a multiple subunit protein complex. Finally, the phenotypes of double rubber-band mutant combinations suggest that the rubber-band mutations affect a neurogenic rather than a myogenic input in excitation-contraction coupling in muscle.
منابع مشابه
sup-9, sup-10, and unc-93 may encode components of a two-pore K+ channel that coordinates muscle contraction in Caenorhabditis elegans.
Genetic studies of sup-9, unc-93, and sup-10 strongly suggest that these genes encode components of a multi-subunit protein complex that coordinates muscle contraction in Caenorhabditis elegans. We cloned sup-9 and sup-10 and found that they encode a two-pore K+ channel and a novel transmembrane protein, respectively. We also found that UNC-93 and SUP-10 colocalize with SUP-9 within muscle cell...
متن کاملCellular/Molecular sup-9, sup-10, and unc-93 May Encode Components of a Two-Pore K Channel that Coordinates Muscle Contraction in Caenorhabditis elegans
Genetic studies of sup-9, unc-93, and sup-10 strongly suggest that these genes encode components of a multi-subunit protein complex that coordinates muscle contraction in Caenorhabditis elegans. We cloned sup-9 and sup-10 and found that they encode a two-pore K channel and a novel transmembrane protein, respectively. We also found that UNC-93 and SUP-10 colocalize with SUP-9 within muscle cells...
متن کاملA visible allele of the muscle gene sup-10X of C. elegans.
In this paper, we extend our previous analyses of a set of genes in Caenorhabditis elegans that are involved in muscle structure and function: unc-93 III, sup-9 II, sup-10 X and sup-11 I. We describe an unusual, visible allele of sup-10, examine how this allele interacts genetically with mutations in other genes of this set and propose that the wild-type products of the unc-93 and sup-10 loci m...
متن کاملThe Caenorhabditis elegans Iodotyrosine Deiodinase Ortholog SUP-18 Functions through a Conserved Channel SC-Box to Regulate the Muscle Two-Pore Domain Potassium Channel SUP-9
Loss-of-function mutations in the Caenorhabditis elegans gene sup-18 suppress the defects in muscle contraction conferred by a gain-of-function mutation in SUP-10, a presumptive regulatory subunit of the SUP-9 two-pore domain K(+) channel associated with muscle membranes. We cloned sup-18 and found that it encodes the C. elegans ortholog of mammalian iodotyrosine deiodinase (IYD), an NADH oxida...
متن کاملDominant suppressors of a muscle mutant define an essential gene of Caenorhabditis elegans.
The sup-11 1 locus of C. elegans was defined by rare dominant suppressors of unc-93(e1500) III, a mutation that affects muscle structure. All ten of these dominant suppressors have a recessive "scrawny" phenotype. Two additional classes of sup-11 alleles were identified. One class, null alleles, was obtained by reversion of the dominant suppressor activity. These null alleles are recessive embr...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Genetics
دوره 135 1 شماره
صفحات -
تاریخ انتشار 1993