1. MicroRNA Pathways In C. elegans Development
University of
Massachusetts
Medical School
RNA Therapeutics
Institute (RTI)
MicroRNA Pathways In C. elegans Development
Developmental Robustness

2. Regulation of Gene Expression by Animal MicroRNAs
Invertebrates:
~150 microRNA genes
Vertebrates:
~1000 microRNA genes
microRNA
gene
Inhibition of protein production
from mRNA targets
Pri-microRNA GW
Effectors
AGO An
Modulators
NHL
AGO
AGO
miRNP
Pre-microRNA

3. How Did/Do MicroRNAs Evolve?
Hsa-mir-100 AACCCGUAGAUCCGAACUUGUG
Cel-mir-52 CACCCGUACAUAUGUUUCCGUGCU
UGAGGUAGUAGGUUGUAUAGUU
UGAGGUAGUAGGUUGUGUGGUU
UGAGGUAGUAGGUUGUAUGGUU
AGAGGUAGUAGGUUGCAUAGU-
UGAGGUAGGAGGUUGUAUAGU-
UGAGGUAGUAGAUUGUAUAGUU
UGAGGUAGUAGUUUGUACAGU-
UGAGGUAGUAGUUUGUGCUGU-
Human let-7-Family
UGAGGUAGGCUCA-GUAGAUGC
UGAGGUAGUAUGUAAUAUUGUA
UGAGGUAGGUGCGAGAAAUGA-
Worm let-7-Family
One Pan-Eumetazoan family 1
lancelet
human
fly
beetle
roundworm
sea anenome
mir-100
let-7
mir-125
> 35 novel Pan-Bilaterian families
lancelet
human
fly
beetle
roundworm
sea anenome
mir-100
let-7
mir-125
MicroRNAs are
Endogenous RNAi
Agents
lancelet
human
fly
beetle
roundworm
sea anenome
~150
~800
RNAi
Eumetazoa
Animals
sponge
~10
>100
Plants
weed
~10
Fungi
mould

4. Evolutionary fluidity of target gene sets
Explicitly-Homologous
Worm
Fly
Human
Chen and rajewsky CSHS 2006
hsa-miR-1 UGGAAUGUAAAGAAGUAUGUAU
cel-miR-1 UGGAAUGUAAAGAAGUAUGUA
dme-miR-1 UGGAAUGUAAAGAAGUAUGGAG
Chen and Rajewsky CSHS 2006

5. Evolution of MicroRNA-Target Interactions
Explicitly-Homologous
Functionally-Analogous
HBL-1
differentiation
let-60/Ras
LIN-41
C. elegans hypodermal lineages
LIN-28
let-7
let-7
human cells
normal
Hmga2
tumor
Mayr, Hemann and Bartel, 2007

6. Functions of microRNA genes in C. elegans
lin-4 and let- 7 control developmental timing (1993, 1999).
••••• Single gene visible phenotypes •••••
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Curr Biol Jul 27;20(14): Epub 2010 Jun 24.
Brenner JL, Jasiewicz KL, Fahley AF, Kemp BJ, Abbott AL.
Loss of individual microRNAs causes mutant phenotypes in sensitized genetic backgrounds in C. elegans.
Department of Biological Sciences, Marquette University, Milwaukee, WI 53201, USA.
Comment in:
Curr Biol Jul 27;20(14):R
MicroRNAs (miRNAs) are small, noncoding RNAs that regulate the translation and/or stability of their mRNA targets. Previous work showed that for most miRNA genes of C. elegans, single-gene knockouts did not result in detectable mutant phenotypes. This may be due, in part, to functional redundancy between miRNAs. However, in most cases, worms carrying deletions of all members of a miRNA family do not display strong mutant phenotypes. They may function together with unrelated miRNAs or with non-miRNA genes in regulatory networks, possibly to ensure the robustness of developmental mechanisms. To test this, we examined worms lacking individual miRNAs in genetically sensitized backgrounds. These include genetic backgrounds with reduced processing and activity of all miRNAs or with reduced activity of a wide array of regulatory pathways. With these two approaches, we identified mutant phenotypes for 25 out of 31 miRNAs included in this analysis. Our findings describe biological roles for individual miRNAs and suggest that the use of sensitized genetic backgrounds provides an efficient approach for miRNA functional analysis.
Curr Biol February 23; 20(4): 367–373.
PMCID: PMC
Published online 2010 January 21. doi: /j.cub
HHMIMSID: HHMIMS185696
Copyright notice and Disclaimer
Many families of Caenorhabditis elegans microRNAs are not essential for development or viability
Howard Hughes Medical Institute, Department of Biology, MIT, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
Ezequiel Alvarez-Saavedra and H. Robert Horvitz
Corresponding author. FAX (617)
The publisher's final edited version of this article is available at Curr Biol
See other articles in PMC that cite the published article.
 Other Sections▼
Publisher's Disclaimer
Summary
Results and Discussion
Experimental Procedures
Supplementary Material
References
MicroRNAs (miRNAs) are approximately 23 nt regulatory RNAs that posttranscriptionally inhibit the functions of protein-coding mRNAs. We previously found that most C. elegans miRNAs are individually not essential for development or viability and proposed that paralogous miRNAs might often function redundantly 1. To test this hypothesis, we generated mutant C. elegans strains that each lack multiple or all members of one of 15 miRNA families

7. C. elegans “Heterochronic” Mutants
Wild type
lin-4(e912)
(Chalfie et al, 1980)
Here’s what it looks like (picture)
Look closer….. What’s wrong with it
Compare it to normal C. elegans (the “wild type”)

8. Retarded Development of lin-4 mutants
Wild Type

9. Adult Alae Formation at L4 Molt
LIN-14 over-expression
L4 Molt
L3 Molt
lin-4
lin-14 3’ UTR Deletion

10. Utterly Robust Cell Fate Specification and Execution
lin-4 and let-7 microRNAs control cell fate progression
Embryo 1
lin-14
lin-4 2
hbl-1
Larval stages
7-Fam 3
let-7
lin-41 4
lin-14 ..C ACCAA C..
UCACA CUCAGGGA
lin AGUGU GAGUCCCU
G A
A C
ACUC
hbl-1 ..A CUUGU U..
AACUA CC GCUACCUUA
UUGAU GG UGAUGGAGU
mir AUGUU A
lin U AUU U..
UUAUACAACC CUGCCUC
GAUAUGUUGG GAUGGAG
let-7 UU AU U
Adult
Adult

11. Genetics of microRNA genes in C. elegans
lin-4 and let- 7 control developmental timing (1993, 1999).
••••• Single gene visible phenotypes •••••
Lucky!
Most Caenorhabditis elegans microRNAs are individually not essential for development or viability.
Miska, Abbott, Alvarez-Saavedra …Bartel, Ambros, Horvitz. PLoS Genet. (2007)
A drag… No
New Phenotypes
The let-7 MicroRNA family … mir-48, mir-84, and mir-241 function together to regulate developmental timing in C. elegans. Abbott et al…Bartel, Horvitz, Ambros. Dev. Cell. (2005)
Redundancy within
a microRNA family
Many families of Caenorhabditis elegans microRNAs are not essential for development or viability
Ezequiel Alvarez-Saavedra and H. Robert Horvitz Curr Biol. 2010
3 of 15 families
are essential
The microRNA miR-1 regulates a MEF-2-dependent retrograde signal at neuromuscular junctions.
Simon et al…Ruvkun, Kaplan, Kim. Cell. (2008)
Stress the worms
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Curr Biol Jul 27;20(14): Epub 2010 Jun 24.
Brenner JL, Jasiewicz KL, Fahley AF, Kemp BJ, Abbott AL.
Loss of individual microRNAs causes mutant phenotypes in sensitized genetic backgrounds in C. elegans.
Department of Biological Sciences, Marquette University, Milwaukee, WI 53201, USA.
Comment in:
Curr Biol Jul 27;20(14):R
MicroRNAs (miRNAs) are small, noncoding RNAs that regulate the translation and/or stability of their mRNA targets. Previous work showed that for most miRNA genes of C. elegans, single-gene knockouts did not result in detectable mutant phenotypes. This may be due, in part, to functional redundancy between miRNAs. However, in most cases, worms carrying deletions of all members of a miRNA family do not display strong mutant phenotypes. They may function together with unrelated miRNAs or with non-miRNA genes in regulatory networks, possibly to ensure the robustness of developmental mechanisms. To test this, we examined worms lacking individual miRNAs in genetically sensitized backgrounds. These include genetic backgrounds with reduced processing and activity of all miRNAs or with reduced activity of a wide array of regulatory pathways. With these two approaches, we identified mutant phenotypes for 25 out of 31 miRNAs included in this analysis. Our findings describe biological roles for individual miRNAs and suggest that the use of sensitized genetic backgrounds provides an efficient approach for miRNA functional analysis.
Curr Biol February 23; 20(4): 367–373.
PMCID: PMC
Published online 2010 January 21. doi: /j.cub
HHMIMSID: HHMIMS185696
Copyright notice and Disclaimer
Many families of Caenorhabditis elegans microRNAs are not essential for development or viability
Howard Hughes Medical Institute, Department of Biology, MIT, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
Ezequiel Alvarez-Saavedra and H. Robert Horvitz
Corresponding author. FAX (617)
The publisher's final edited version of this article is available at Curr Biol
See other articles in PMC that cite the published article.
 Other Sections▼
Publisher's Disclaimer
Summary
Results and Discussion
Experimental Procedures
Supplementary Material
References
MicroRNAs (miRNAs) are approximately 23 nt regulatory RNAs that posttranscriptionally inhibit the functions of protein-coding mRNAs. We previously found that most C. elegans miRNAs are individually not essential for development or viability and proposed that paralogous miRNAs might often function redundantly 1. To test this hypothesis, we generated mutant C. elegans strains that each lack multiple or all members of one of 15 miRNA families
Loss of individual microRNAs causes mutant phenotypes in sensitized genetic backgrounds in C. elegans.
Brenner et al, … Abbott. Curr Biol. (2010)
Visible Phenotypes
for 25 of 31
miRNA genes

12. microRNAs Are Embedded Within Diverse Networks
• Redundancy between microRNA families
microRNAs Are Embedded Within Diverse Networks
mir-34
Gonadal
Morphogenesis
Argonaute
mir-83
• Redundancy with gene regulatory “hubs”
Robustness
thru
Redundancy
Fertility
mir-1
U.S. National Library of Medicine National Institutes of Health
PubMed
Search:All DatabasesPubMedProteinNucleotideGSSESTStructureGenomeBioSampleBioSystemsBooksCancerChromosomesConserved DomainsdbGaPdbVar3D DomainsEpigenomicsGeneGenome ProjectGENSATGEO ProfilesGEO DataSetsHomoloGeneJournalsMeSHNCBI Web SiteNLM CatalogOMIAOMIMPeptidomePMCPopSetProbeProtein ClustersPubChem BioAssayPubChem CompoundPubChem SubstanceSNPSRATaxonomyToolKitToolKitAllUniGeneUniSTS
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Curr Biol Jul 27;20(14): Epub 2010 Jun 24.
Brenner JL, Jasiewicz KL, Fahley AF, Kemp BJ, Abbott AL.
Loss of individual microRNAs causes mutant phenotypes in sensitized genetic backgrounds in C. elegans.
Department of Biological Sciences, Marquette University, Milwaukee, WI 53201, USA.
Comment in:
Curr Biol Jul 27;20(14):R
MicroRNAs (miRNAs) are small, noncoding RNAs that regulate the translation and/or stability of their mRNA targets. Previous work showed that for most miRNA genes of C. elegans, single-gene knockouts did not result in detectable mutant phenotypes. This may be due, in part, to functional redundancy between miRNAs. However, in most cases, worms carrying deletions of all members of a miRNA family do not display strong mutant phenotypes. They may function together with unrelated miRNAs or with non-miRNA genes in regulatory networks, possibly to ensure the robustness of developmental mechanisms. To test this, we examined worms lacking individual miRNAs in genetically sensitized backgrounds. These include genetic backgrounds with reduced processing and activity of all miRNAs or with reduced activity of a wide array of regulatory pathways. With these two approaches, we identified mutant phenotypes for 25 out of 31 miRNAs included in this analysis. Our findings describe biological roles for individual miRNAs and suggest that the use of sensitized genetic backgrounds provides an efficient approach for miRNA functional analysis.
Curr Biol February 23; 20(4): 367–373.
PMCID: PMC
Published online 2010 January 21. doi: /j.cub
HHMIMSID: HHMIMS185696
Copyright notice and Disclaimer
Many families of Caenorhabditis elegans microRNAs are not essential for development or viability
Howard Hughes Medical Institute, Department of Biology, MIT, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
Ezequiel Alvarez-Saavedra and H. Robert Horvitz
Corresponding author. FAX (617)
The publisher's final edited version of this article is available at Curr Biol
See other articles in PMC that cite the published article.
 Other Sections▼
Publisher's Disclaimer
Summary
Results and Discussion
Experimental Procedures
Supplementary Material
References
MicroRNAs (miRNAs) are approximately 23 nt regulatory RNAs that posttranscriptionally inhibit the functions of protein-coding mRNAs. We previously found that most C. elegans miRNAs are individually not essential for development or viability and proposed that paralogous miRNAs might often function redundantly 1. To test this hypothesis, we generated mutant C. elegans strains that each lack multiple or all members of one of 15 miRNA families
Loss of individual microRNAs causes mutant phenotypes in sensitized genetic backgrounds in C. elegans.
Brenner et al, 2010

13. Distinct MicroRNAs with Convergent Targets Gonadal Morphogenesis
Buffering morphogenetic processes against temperature changes
B-integrin
PAT-3
PEB-1
mir-34
mir-83
pat-3 mRNA
Buffered against
Temperature changes
Gonadal
Morphogenesis
peb-1 mRNA
Transcription factor
Samantha Burke & Molly Hammell

14. Hermaphrodite Gonad Morphogenesis in C. elegans
Phase 1
Phase 2
Phase 3
From Worm Atlas

15. Migration Defects in mir-34 (-/-) and mir-83 (-/-) Mutants
Samantha Burke & Molly Hammell

16. Taking a Cue from Richard Carthew….
Drosophila mir-7 Buffers Eye Development Against Temperature Changes
Li et al., Carthew Cell (2):

17. Temperature Oscillations Aggravate mir-34 & mir-83 Phenotypes
Constant 20 ℃
15oC – 25oC Oscillations (8 hr)
Samantha Burke & Molly Hammell

18. Samantha Burke & Molly Hammell
*** 54
% defective gonadal migration 19 14 2
mir-83(+)
mir-83(0)
mir-83(+)
mir-83(0)
mir-34(+)
mir-34(+)
mir-34(0)
mir-34(0)
Samantha Burke & Molly Hammell

19. Distinct MicroRNAs with Convergent Targets Gonadal Morphogenesis
Buffering morphogenetic processes against temperature changes
B-integrin
PAT-3
PEB-1
mir-34
mir-83
pat-3 mRNA
Buffered against
Temperature changes
Gonadal
Morphogenesis
peb-1 mRNA
Transcription factor
Samantha Burke & Molly Hammell

20. Modulation of microRNA levels and (lin-4) activity
Reprogramming of HBL-1 microRNA regulation by life history
Post-dauer:
mir-48, mir-84, mir-241, let-7
lin-4: MAJOR Role
mir-48, mir-84, mir-241, let-7
lin-4: minor role
Continuous:
NHL-2
AGO An
let-7
Family
lin-4
HBL-1 mRNA
Modulation of microRNA levels and (lin-4) activity
Xantha Karp

21. Accommodation of Stress and Diapause in C. elegans Development
Unfavorable
Favorable
Dauer-
interrupted 1
Insulin/IGF
DAF-16/Fox0 2
Dauer
larva
Larval stages 3 4
Adult
Continuous

22. Utterly Robust Cell Fate Specification and Execution
lin-4 and let-7 microRNAs control cell fate progression
Embryo 1
lin-14
lin-4 2
hbl-1
Larval stages
7-Fam
(Optional) Developmental Quiescence 3
let-7
lin-41 4
lin-14 ..C ACCAA C..
UCACA CUCAGGGA
lin AGUGU GAGUCCCU
G A
A C
ACUC
lin U AUU U..
UUAUACAACC CUGCCUC
GAUAUGUUGG GAUGGAG
let-7 UU AU U
hbl-1 ..A CUUGU U..
AACUA CC GCUACCUUA
UUGAU GG UGAUGGAGU
mir AUGUU A
Adult
Adult

23. lin-4 and let-7 microRNAs control cell fate progression
Embryo 1
lin-14
lin-4 2
hbl-1
Larval stages
7-Fam
(Optional) Developmental Quiescence 3
Dauer larva
let-7
lin-41 4
Adult
Adult
Robust Timing of cell fates

24. microRNAs in C. elegans cell fate progression Developmental Signals
Adult L1 L2 L4 L3
miR-48
miR-84
miR-241
let-7
lin-4
Wild type
LIN-29
LIN-41
lin-4
let-7
HBL-1
LIN-14 L1 L2 L3 L4 Ad
let-7Fam
mir-48
mir-84
mir-241
LIN-28
Developmental Signals
Dauer Larva Quiescence
Robustness of L2 to L3:
Redundancy of let-7 family microRNAs
Shared regulationof hbl by lin-4 and let-7 fam
MicroRNA
pathways
Transcription
Factors
Robust Timing of cell fates

25. Dosage-Sensitive activity of let-7-Family microRNAs
UGAGGUAGUAGGUUGUAUAGUU
UGAGGUAGGCUCA-GUAGAUGC
UGAGGUAGUAUGUAAUAUUGUA
UGAGGUAGGUGCGAGAAAUGA-
Worm let-7-Family
Wild type
let-7-Fam -1 L1 L1 L2 L3 L4 Ad
lin-4
LIN-14
LIN-28 L2
let-7Fam
mir-48
mir-84
mir-241
let-7
HBL-1
Developmental Signals L3 L4
let-7
LIN-41
LIN-29 Ad

26. Dosage-Sensitive activity of let-7-Family microRNAs
UGAGGUAGUAGGUUGUAUAGUU
UGAGGUAGGCUCA-GUAGAUGC
UGAGGUAGUAUGUAAUAUUGUA
UGAGGUAGGUGCGAGAAAUGA-
Worm let-7-Family
let-7-Fam -3
Wild type L1 L1 L2 L3 L4 Ad
lin-4
LIN-14
LIN-28 L2
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
HBL-1
Developmental Signals L3 L4 Ad L3 L4 L2
let-7
LIN-41
LIN-29
Normal
Retarded
Adult-specific col-19::GFP

27. Retarded phenotype of let-7-Fam -3 mutant
Adult-specific col-19::GFP
Normal Adult
Retarded Adult

28. Stressful environment Developmental Signals
Post-dauer Development of let-7-Fam -3 mutant
let-7-Fam -3
let-7-Fam -3
Stressful environment
Healthy environment L1
lin-4
LIN-14
LIN-28 L2
HBL-1
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
Developmental Signals
Dauer Larva Quiescence Ad L3 L4 L2 L3 L4
let-7
LIN-41
LIN-29
Normal
Retarded
“Post-dauer” Suppression

29. Adult-expression of col-19::GFP
Post-Dauer Suppression of let-7-Fam -3 Phenotypes
Wild Type
let-7-Fam-3
Continuous
Post-dauer
Continuous
Post-dauer
Adult-expression of col-19::GFP

30. Stressful environment
Post-dauer Suppression of let-7-Fam -3 Phenotypes
let-7-Fam -3
let-7-Fam -3
High Pheromone
Low Pheromone
Healthy environment
Stressful environment L1
lin-4
LIN-14
LIN-28 L2
Mod
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
Developmental Signals
Dauer Larva Quiescence Ad L3 L4
let-7
LIN-41
LIN-29
Normal
Retarded
Xantha Karp
Post-Dauer Suppression

31. Developmental Signals
Gene products required for Post-dauer Suppression
Mod(0); let-7-Fam -3
let-7-Fam -3
let-7-Fam -3
High Pheromone
Low Pheromone L1
lin-4
LIN-14
LIN-28 L2
Mod
HBL-1
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
Developmental Signals
Dauer Larva Quiescence Ad L3 L4 L2 L3 L4
let-7
LIN-41
LIN-29
Retarded
Normal
Retarded
Xantha Karp
Post-Dauer Suppression

32. Developmental Signals
NHL-2/TRIM32 is required for Post-dauer Suppression
let-7-Fam -3
let-7-Fam -3
High Pheromone
Low Pheromone L1
lin-4
LIN-14
LIN-28 L2
NHL-2
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
Developmental Signals
Dauer Larva Quiescence Ad L3 L4
let-7
LIN-41
LIN-29
Normal
Retarded
Xantha Karp
“Post-Dauer” Suppression

33. Developmental Signals
NHL-2/TRIM32 is required for Post-dauer Suppression
nhl-2(0); let-7-Fam -3
nhl-2(0); let-7-Fam -3
High Pheromone
Low Pheromone L1
lin-4
LIN-14
LIN-28 L2
NHL-2
HBL-1
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
Developmental Signals
Dauer Larva Quiescence Ad L3 L4 L2 L3 L4
let-7
LIN-41
LIN-29
Retarded
Normal
Retarded
Xantha Karp
“Post-Dauer” Suppression

34. Col-19::GFP expression in Post-Dauer Adults
NHL-2/TRIM32 is required for Post-dauer Suppression
Col-19::GFP expression in Post-Dauer Adults
Post-Dauer let-7-Fam-3
Post-Dauer
nhl-2; let-7-Fam-3

35. Developmental Signals
lin-4 microRNA is required for Postdauer Suppression
lin-4(0); let-7-Fam -3
let-7-Fam -3
lin-4(0); let-7-Fam -3
let-7-Fam -3
High Pheromone
Low Pheromone L1
lin-4
LIN-14
LIN-28 L2
NHL-2
HBL-1
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
Developmental Signals
Dauer Larva Quiescence Ad L3 L4 L2 L3 L4
let-7
LIN-41
LIN-29
Retarded
Normal
Retarded
Xantha Karp
“Post-Dauer” Suppression

36. HBL-1::GFP::UTR-HBL-1 lin-4 is required for down regulation of HBL-1
Between L2 and Post Dauer L3 L1 L2
Dauer larva
Post Dauer L3 WT WT WT WT
Post Dauer L3
let-7-Fam-3 L1 L2
Dauer larva
Post Dauer L3
Down Regulated
HBL-1::GFP::UTR-HBL-1
lin-4; let-7-Fam-3
Not Down Regulated

37. Developmental Signals
lin-4 function is More Critical after Dauer Larva Quiescence
lin-4(0); let-7-Fam -1
let-7-Fam -1
lin-4(0); let-7-Fam -1
let-7-Fam -1
High Pheromone
Low Pheromone L1
lin-4
LIN-14
LIN-28 L2 L2
NHL-2
HBL-1
HBL-1
let-7Fam
mir-48
mir-84
mir-241
let-7
Developmental Signals
Dauer Larva Quiescence Ad L3 L4 L2 L3 L4 Ad L3 L4
let-7
LIN-41
LIN-29
Retarded
Normal
Xantha Karp

38. lin-4 microRNA is More Critical after Dauer Larva Quiescence
Continuous
mir-84(0)
Post-Quiescence **
lin-4(0); mir-84(0)
Continuous **
Post-Quiescence
** P < 0.01
% Adults expressing larval cell fates
*All strains contain lin-14(n179)
Xantha Karp

39. Dauer Traversing vs Continuously-Developing
Developmental profiles of lin-4 and let-7-Family microRNAs
Taqman Q-RT/PCR
Dauer Traversing vs Continuously-Developing
lin-4
mir-84
let-7
mir-241
mir-48
microRNA abundance
Dauer vs Continuous
1.0
L2D/L2
Dauer/L2m
PDL3/L3
PDL4/L4

40. Modulation of microRNA levels and (lin-4) activity
Reprogramming of HBL-1 microRNA regulation by life history
Post-dauer:
mir-48, mir-84, mir-241, let-7
lin-4: MAJOR Role
Insulin/IGF
DAF-16/Fox0
mir-48, mir-84, mir-241, let-7
lin-4: minor role
Continuous:
NHL-2
AGO An
let-7
Family
lin-4
HBL-1 mRNA
Modulation of microRNA levels and (lin-4) activity
Xantha Karp

41. Physiological Modulation of microRNA activity
Enhancers and suppressors of
let-7-Family loss-of-function mutations
Zhiji Ren, Chris Hammell
col-19
Alae
Description
rab-7
enhance
endosomal trafficking
vps-11
vps-33.1/33.2
suppress
pqn-29
prion like gene
pqn-67
C01A2.4 (CHMP2B)
ESCRT complex
nhl-2
miRISC modulator
cgh-1
miRISC essential component
lin-46
scaffolding protein

42. Physiological Modulation of microRNA activity
Bacterial Diet
Zhiji Ren

43. let-7-Family microRNAs in Diet and Development Developmental cell fate
Bacterial Quality/Toxicity
Metabolic
Signaling
Innate Immunity
Developmental cell fate
specification
mir-84
let-7
Buffering against
food stress
mir-48
mir-241

44. Developmental Timing, Robustness and Stress Responses
Current:
Former:
Zhiji Ren
Molly Hammell
Chris Hammell
Samantha Burke
Xantha Karp
Omid Harandi
Sungwook Choi
LIN-28 Function
Rosalind Lee
Circulating microRNAs
in human plasma and CSF
Katie McJunkin
Regulation of microRNA stability/turnover
Maria Ow
MicroRNAs in diverse stress responses
Catherine Sterling
microRNAs and long noncoding RNAs
Elizabeth Thatcher
Alexey Wolfson
Anna Zinovyeva