Transmembrane protein 57, TMEM57, Polyclonal primary Antibodies
- Known as:
- Transmembrane protein 57, TMEM57, Polyclonal captor Antibodies
- Catalog number:
- BPA1102
- Product Quantity:
- 100 μg
- Category:
- -
- Supplier:
- Biospect
- Gene target:
- Transmembrane protein 57 TMEM57 Polyclonal primary Antibodies
Ask about this productRelated genes to: Transmembrane protein 57, TMEM57, Polyclonal primary Antibodies
- Gene:
- MACO1 NIH gene
- Name:
- macoilin 1
- Previous symbol:
- TMEM57
- Synonyms:
- FLJ10747
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-22
- Date modifiied:
- 2017-10-30
Related products to: Transmembrane protein 57, TMEM57, Polyclonal primary Antibodies
Related articles to: Transmembrane protein 57, TMEM57, Polyclonal primary Antibodies
- In its natural habitat, must distinguish friend from foe. are abundant in the worm's environment and can be nutritious or pathogenic. Previously, we found that worms learn to avoid and through a small RNA (sRNA)-mediated pathway targeting the gene , and this behavior is inherited for four generations. Here, we show that learns to transgenerationally avoid another pathogenic bacteria 15 (PF15). The PF15 sRNA, Pfs1, targets the ephrin receptor through 16 nt of perfect match, suggesting the evolution of a distinct bacterial sRNA/ gene target pair. Knockdown of both induce PF15 avoidance, and loss reduces expression, placing both genes in the sRNA-targeted pathogenic avoidance pathway. Thus, multiple genes in this avoidance pathway can act as targets for bacterial sRNAs, expanding the possibilities for evolution of trans-kingdom regulation of behavior. - Source: PubMed
Publication date: 2025/04/23
Seto Renee JBrown RachelKaletsky RachelParsons Lance RMoore Rebecca SBalch Julia MGitai ZemerMurphy Coleen T - The burgeoning field of environmental epigenetics has revealed the malleability of the epigenome and uncovered numerous instances of its sensitivity to environmental influences; however, pinpointing specific mechanisms that tie together environmental triggers, epigenetic pathways, and organismal responses has proven difficult. This article describes how Caenorhabditis elegans can fill this gap, serving as a useful model for the discovery of molecular epigenetic mechanisms that are conserved in humans. - Source: PubMed
Publication date: 2025/01/20
Filipowicz AdamAllard Patrick - are exposed to a variety of pathogenic and non-pathogenic bacteria species in their natural environment. Correspondingly, has evolved an ability to discern between nutritive and infectious bacterial food sources. Here we show that can learn to avoid the pathogenic bacteria (PF15), and that this learned avoidance behavior is passed on to progeny for four generations, as we previously demonstrated for (PA14) and , using similar mechanisms, including the involvement of both the TGF-β ligand DAF-7 and retrotransposon-encoded virus-like particles. PF15 small RNAs are both necessary and sufficient to induce this transgenerational avoidance behavior. Unlike PA14 or , PF15 does not use P11, Pv1, or a small RNA with homology for this avoidance; instead, an unrelated PF15 small RNA, Pfs1, that targets the Ephrin receptor gene is necessary and sufficient for learned avoidance, suggesting the evolution of yet another bacterial sRNA/ gene target pair involved in transgenerational inheritance of pathogen avoidance. As VAB-2 Ephrin receptor ligand and MACO-1 knockdown also induce PF15 avoidance, we have begun to understand the genetic pathway involved in small RNA targeted pathogenic avoidance. Moreover, these data show that axon guidance pathway genes (VAB-1 and VAB-2) have previously unknown adult roles in regulating neuronal function. may have evolved multiple bacterial specificity-encoded small RNA-dependent mechanisms to avoid different pathogenic bacteria species, thereby providing progeny with a survival advantage in a dynamic environment. - Source: PubMed
Publication date: 2024/05/23
Seto ReneeBrown RachelKaletsky RachelParsons Lance RMoore Rebecca SMurphy Coleen T - C. elegans can learn to avoid pathogenic bacteria through several mechanisms, including bacterial small RNA-induced learned avoidance behavior, which can be inherited transgenerationally. Previously, we discovered that a small RNA from a clinical isolate of Pseudomonas aeruginosa, PA14, induces learned avoidance and transgenerational inheritance of that avoidance in C. elegans. Pseudomonas aeruginosa is an important human pathogen, and there are other Pseudomonads in C. elegans' natural habitat, but it is unclear whether C. elegans ever encounters PA14-like bacteria in the wild. Thus, it is not known if small RNAs from bacteria found in C. elegans' natural habitat can also regulate host behavior and produce heritable behavioral effects. Here we screened a set of wild habitat bacteria, and found that a pathogenic Pseudomonas vranovensis strain isolated from the C. elegans microbiota, GRb0427, regulates worm behavior: worms learn to avoid this pathogenic bacterium following exposure, and this learned avoidance is inherited for four generations. The learned response is entirely mediated by bacterially-produced small RNAs, which induce avoidance and transgenerational inheritance, providing further support that such mechanisms of learning and inheritance exist in the wild. We identified Pv1, a small RNA expressed in P. vranovensis, that has a 16-nucleotide match to an exon of the C. elegans gene maco-1. Pv1 is both necessary and sufficient to induce learned avoidance of Grb0427. However, Pv1 also results in avoidance of a beneficial microbiome strain, P. mendocina. Our findings suggest that bacterial small RNA-mediated regulation of host behavior and its transgenerational inheritance may be functional in C. elegans' natural environment, and that this potentially maladaptive response may favor reversal of the transgenerational memory after a few generations. Our data also suggest that different bacterial small RNA-mediated regulation systems evolved independently, but define shared molecular features of bacterial small RNAs that produce transgenerationally-inherited effects. - Source: PubMed
Publication date: 2024/03/28
Sengupta TitasSt Ange JonathanKaletsky RachelMoore Rebecca SSeto Renee JMarogi JacobMyhrvold CameronGitai ZemerMurphy Coleen T - Previously, we discovered that a small RNA from a clinical isolate of PA14, induces learned avoidance and its transgenerational inheritance in . is an important human pathogen, and there are other in natural habitat, but it is unclear whether ever encounters PA14-like bacteria in the wild. Thus, it is not known if small RNAs from bacteria found in natural habitat can also regulate host behavior and produce heritable behavioral effects. Here we found that a pathogenic strain isolated from the microbiota, GRb0427, like PA14, regulates worm behavior: worms learn to avoid this pathogenic bacterium following exposure to GRb0427, and this learned avoidance is inherited for four generations. The learned response is entirely mediated by bacterially-produced small RNAs, which induce avoidance and transgenerational inheritance, providing further support that such mechanisms of learning and inheritance exist in the wild. Using bacterial small RNA sequencing, we identified Pv1, a small RNA from GRb0427, that matches the sequence of . We find that Pv1 is both necessary and sufficient to induce learned avoidance of Grb0427. However, Pv1 also results in avoidance of a beneficial microbiome strain, ; this potentially maladaptive response may favor reversal of the transgenerational memory after a few generations. Our findings suggest that bacterial small RNA-mediated regulation of host behavior and its transgenerational inheritance are functional in natural environment, and that different bacterial small RNA-mediated regulation systems evolved independently but define shared molecular features of bacterial small RNAs that produce transgenerationally-inherited effects. - Source: PubMed
Publication date: 2023/10/17
Sengupta TitasSt Ange JonathanMoore RebeccaKaletsky RachelMarogi JacobMyhrvold CameronGitai ZemerMurphy Coleen T