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7 publications mentioning cel-mir-51

Open access articles that are associated with the species Caenorhabditis elegans and mention the gene name mir-51. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 246
Therefore, we tested whether the mir-51 family interacted with additional miRNA-regulated pathways by determining if loss of mir-51 family members could suppress other miRNA mutant phenotypes that are distinct from developmental timing, including regulation of neuronal asymmetry, let-7 family regulation of vulva cell fate specification, regulation of defecation, mir-35 family regulation of embryonic development and regulation of neuromuscular function. [score:11]
Loss of mir-51 family members partially suppresses retarded developmental timing phenotypesThe loss of mir-51 family members suppresses alg-1 developmental timing defects [17], suggesting a possible direct role in the regulation of the developmental timing pathway. [score:10]
Loss of mir-51 family members suppresses additional miRNA -dependent regulatory pathways in C. elegans Genetic interactions with the developmental timing pathway may reflect a specific function for the mir-51 family miRNAs in the regulation of targets in this pathway. [score:8]
We propose that the broad activity of mir-51 family members reflects the repression of a target or multiple target mRNAs that act in distinct genetic pathways, possibly acting to fine tune, or buffer target protein levels. [score:7]
These activities for the mir-51 family may reflect the regulation of a single target that functions broadly in many pathways or the regulation of multiple targets that each function in distinct pathways. [score:7]
A direct target or targets of the mir-51 family in the diverse development pathways described herein remain unknown. [score:7]
The loss of mir-51 family members suppresses alg-1 developmental timing defects [17], suggesting a possible direct role in the regulation of the developmental timing pathway. [score:7]
First, unlike other developmental timing miRNAs, such as lin-4 and let-7, mir-51 family members do not display stage-specific expression but rather display nearly ubiquitous expression throughout development. [score:7]
Unlike other genes that regulate developmental timing, mir-51 family members are expressed broadly and abundantly throughout the life of the worm [25]– [29]. [score:5]
These results indicate that the observed suppression of developmental timing defects is not likely due to an increase in overall miRNA levels and that mir-51 family miRNAs likely do not function broadly to regulate miRNA biogenesis. [score:5]
If the mir-51 family opposes let-7 activity in vulva development, as it did in the developmental timing pathway, then it would be expected that loss of mir-51 family members should suppress the let-60gf Muv phenotype. [score:5]
Because the mir-51 family is broadly and abundantly expressed throughout development in C. elegans [25]– [28], multiple binding sites for the mir-51 family within the 3′UTR of a gene would be expected to cause robust repression of that gene throughout development. [score:5]
Genetic interactions with the developmental timing pathway may reflect a specific function for the mir-51 family miRNAs in the regulation of targets in this pathway. [score:5]
Instead, we propose that the mir-51 family functions to regulate multiple targets in diverse developmental pathways in C. elegans. [score:5]
Of the 293 conserved targets predicted by Targetscan [52], [53], only 6 contain more than one binding site for the mir-51 family and none of these 6 have more than two binding sites for the mir-51 family. [score:5]
Our analysis of candidate targets failed to conclusively identify downstream mir-51 family targets (data not shown). [score:5]
Loss of mir-51 family members does not broadly enhance miRNA biogenesis or activityTo account for the observation that the loss of mir-52 suppressed multiple miRNA -dependent phenotypes, we proposed that mir-52 may act to broadly regulate miRNA biogenesis or activity. [score:4]
Loss of mir-51 family members partially suppresses these developmental timing defects in alg-1 worms [17]. [score:4]
Next, we examined the effect of elevated expression of mir-51 family members on the retarded development of mir-48 mir-241 (mir-48/241) mutant worms. [score:4]
Loss of mir-51 family members suppresses additional miRNA -dependent regulatory pathways in C. elegans. [score:4]
We therefore propose that the mir-51 family miRNAs are not themselves regulators of developmental timing decisions but that they likely act downstream in the execution phase of developmental programs. [score:4]
mir-51 family members function upstream of hbl-1, but not lin-28, to suppress developmental timing defects in let-7 family mutants. [score:4]
mir-52/53/54/55/56 mutant worms display impenetrant embryonic lethality, slow growth, and mating defects [13], [25] indicating that mir-51 family targets are sufficiently misregulated to result in severe, penetrant mutant phenotypes. [score:4]
Because the alg-1 developmental timing defects are similar to those associated with the loss of the let-7 family miRNAs [18], we determined if loss of individual mir-51 family members was sufficient to suppress let-7 timing defects. [score:4]
These pleiotropic phenotypes indicate that mir-51 family members likely function to regulate multiple downstream targets and pathways. [score:4]
mir-51 family members function upstream of hbl-1, but not lin-28, to suppress developmental timing defects in let-7 family mutantsGenetic interactions between mir-52 and let-7 family members as well as hbl-1(ve18) suggest that mir-52 may act upstream of hbl-1 to promote its activity. [score:4]
The mechanism whereby loss of individual mir-51 family members suppresses alg-1 developmental timing defects is unclear. [score:4]
Additionally, we report that the mir-51 family interacts with multiple, diverse, miRNA regulated genetic pathways, including pathways regulated by the let-7 and mir-35 family miRNAs, as well as, miR-240/786, and miR-1. We provide evidence that is inconsistent with the mo del that the mir-51 family regulates miRNA biogenesis or miRNA activity. [score:4]
The goal of this study was to define the mechanism whereby loss of mir-51 family members can suppress the developmental timing defects of alg-1 mutant worms. [score:4]
Loss of mir-51 family members partially suppresses retarded developmental timing phenotypes. [score:4]
We determined if the loss of mir-51 family members can suppress the phenotypes of lin-46 and puf-9, mutants that display retarded developmental timing defects [30], [31]. [score:4]
Although mir-51 family members interact with developmental timing genes, such as let-7 family members and lin-46, mir-51 family members are atypical developmental timing genes. [score:3]
Our genetic evidence indicates that mir-51 family members act early in the developmental timing pathway to regulate L2 versus L3 cell fate decisions. [score:3]
This indicates elevated expression of mir-51 family members enhances the L2 repetition phenotype. [score:3]
Although this clustered organization in the genome is not observed in worms, evidence herein supports a functional relationship between the let-7 and mir-51 family of miRNAs in the regulation of the developmental timing pathway. [score:3]
Loss of the mir-51 family member, mir-52, partially suppressed the vulva cell fate defects of let-60gf mutants, the ASEL cell fate defects of mutants, the defecation defects of mutants, and the levamisole resistance of mutants. [score:3]
Consistent with this mo del, the miR-51 family is both abundantly [26]– [28] and broadly expressed in tissues in which we observed a genetic interaction, including the hypodermis, the ASEL neuron, the vulva, the intestine, and muscle [25], [29], [45], [46]. [score:3]
We observed that loss of the mir-51 family member, mir-52, strongly suppressed the L2 stage reiteration phenotype of mir-48/84/241 mutants and lin-46 mutants. [score:3]
Together, these data indicate that the mir-51 family functions to regulate the execution of the L3 stage program, acting either downstream or in parallel to the let-7 family miRNAs and lin-46 and may have additional activity in the control of alae formation in late larval development. [score:3]
Loss of mir-51 family members did not suppress either of these phenotypes in let-7 mutants (Table 1). [score:3]
This suggests that puf-9 may function downstream of the mir-51 family to regulate developmental timing. [score:3]
Identification of mir-51 family targets in the vulva specification pathway is required to elucidate the functions of individual mir-51 family members. [score:3]
The enhancement of the precocious developmental timing defects observed in mir-48(ve33), hbl-1(ve18), and lin-14(n179ts) mutant worms is consistent with a role for the mir-51 family in the regulation of L2 versus L3 cell fate decisions. [score:3]
We therefore wanted to determine the function of the mir-51 family members in the regulation of the developmental timing pathway. [score:3]
We speculate that the function of mir-51 family members may be to weakly repress or fine-tune the protein levels for a large set of diverse downstream targets. [score:3]
We found that the interactions with multiple miRNA -dependent pathways likely does not reflect the regulation of the miRNA pathway by the mir-51 family. [score:2]
0037185.g003 Figure 3The mir-51 family members, mir-52 and mir-54/55/56, function in multiple miRNA -dependent developmental pathways. [score:2]
This may reflect distinct activities of individual mir-51 family members in the control of vulva development. [score:2]
Genetic interactions of mir-51 family with precocious developmental timing mutants. [score:2]
To accomplish this, we used mjEx160, an extrachromosomal array with the genomic fragment for mir-54/55/56 that was previously shown to rescue the embryonic lethality of mir-51 family mutant worms [25] and the developmental timing phenotypes in mir-54/55/56 alg-1 mutant worms [17]. [score:2]
Here, we have defined the genetic interactions of mir-51 family members with components of the developmental timing pathway. [score:2]
Loss of the other mir-51 family members had no significant effect on lin-46 developmental timing defects (data not shown). [score:2]
However, mutants lacking individual mir-51 family members did not display developmental timing abnormalities such as defects in alae formation or defects in seam cell divisions (Table 1 and Table 2). [score:2]
Alternatively, these interactions may reflect a broader function for the mir-51 family in the regulation of miRNA biogenesis or activity. [score:2]
These data indicate that activity is not enhanced in the absence of mir-52, thereby suggesting that the mir-51 family does not function broadly to regulate the activity of miRNAs. [score:2]
Together, these data are consistent with the mir-51 family functioning downstream or in parallel to lin-28, lin-46 and the let-7 family, but upstream of hbl-1 to regulate the L2 versus L3 cell fate decisions. [score:2]
In addition, loss of nearly all mir-51 family members, which results in multiple defects including slow growth and embryonic lethality, did not result in developmental timing defects [13,25; Table 1 and Table 2]. [score:2]
Genetic interactions of the mir-51 family with retarded developmental timing mutants. [score:2]
Thus, mir-51 family members likely do not function to regulate the core pathway required for all miRNA biogenesis or activity. [score:2]
In C. elegans, the mir-51 family comprises six miRNAs, miR-51 through miR-56. [score:1]
However, it remains possible that mir-51 family members may function to modulate miRNA activity in specific cells or for only a subset of miRNAs not included in our analysis. [score:1]
mir-1. Loss of mir-51 family members does not broadly enhance miRNA biogenesis or activity. [score:1]
Further, worms that are multiply mutant for 5 out of 6 members of the mir-51 family, mir-52/53/54/55/56, also do not display alae formation defects (Table 1 and Table 2), despite displaying other mutant phenotypes including slow growth and larval lethality [13], [25]. [score:1]
This broad activity described for the mir-51 family is unlike that of previously described miRNAs in C. elegans. [score:1]
As described above, neither increased miRNA biogenesis nor increased miRNA activity was observed in mir-51 family mutant backgrounds. [score:1]
Levels of mature let-7, miR-58, miR-62, and miR-244 are unchanged in the absence of mir-51 family members. [score:1]
lsy-6. The mir-51 family members, mir-52 and mir-54/55/56. [score:1]
0037185.g004 Figure 4Levels of mature let-7, miR-58, miR-62, and miR-244 are unchanged in the absence of mir-51 family members. [score:1]
Loss of the entire mir-51 family in C. elegans results in embryonic lethality, due to a failure of pharyngeal attachment [25]. [score:1]
The mir-51 family is part of the larger miR-99/100 family, a miRNA family that shows deep conservation from cnidarians through humans [24]. [score:1]
Surprisingly, we found that mir-51 family members displayed genetic interactions with multiple miRNA genes. [score:1]
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[+] score: 5
For example, C. elegans lin-4 and let-7 family members are important for correct larval development, the mir-36 family is essential for embryonic development, the mir-51 family is required for pharynx attachment during embryogenesis and the mir-58 family is involved in regulating locomotion, growth and development of arrested dauer stage larvae (Alvarez-Saavedra and Horvitz, 2010). [score:5]
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[+] score: 3
This family has expanded in some animal lineages: in C. elegans it is referred to as the miR-51 family and is redundantly required for embryonic development [42] and also involved in developmental timing and buccal cavity formation [42, 43]. [score:3]
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[+] score: 2
Exceptions are the early lethality phenotypes resulting from both the combined loss of mir-35- mir-42 [24] and of mir-51-mir-56, [24, 25], as well as the movement and body size defect resulting from combined mutation of mir-58, -80, -81 and -82 [24]. [score:2]
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[+] score: 1
Loss of certain miRNAs or miRNA families led to hypoxia sensitivity (mir-2, mir-35, mir-44, mir-49, mir-51, mir-60, mir-63 and mir-67) and others to hypoxia resistance (let-7, mir-58, mir-67, mir-79, mir-237, mir-246, mir-359). [score:1]
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[+] score: 1
Figure 9 shows an example of a detailed descriptor report for cel-mir-51 for scoring mo del Metazoa. [score:1]
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These included miRNAs cel-miR-70, cel-miR-51, cel-miR-56, cel-miR-230, cel-miR-238, cel-miR-83, etc. [score:1]
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