Effective Poster Design by BC Children's Hospital Research

Effective poster design LEGIBLE, CONCISE, CLEAR AND COMPELLING Martin Krzywinski http://mkweb.bcgsc.ca Canada's Michael Smith Genome Sciences Centre at BC Cancer Vancouver, Canada

Deliver your explanation with the necessary degree of supporting detail and as little ink as possible to encourage the largest number of relevant ideas in the reader.

no clipart no bullet points concise language and

no pie charts

Journal of Neuroscience 30 May 2018, 38 (22) 5182-5195

adopt a constrained style

"Rich, ornate prose is hard to digest, generally unwholesome and sometimes nauseating."

D A A

Krzywinski, M., Elements of visual style. Nat Methods, 2013. 10(5): p. 371.

E Cancer

A A

C K3

Krzywinski, M., Elements of visual style. Nat Methods, 2013. 10(5): p. 371.

C AN C E R

D A A

Cancer

K3 A A

C K3

Krzywinski, M., Elements of visual style. Nat Methods, 2013. 10(5): p. 371.

CA NCER

gestalt

An organized whole that is perceived as more than the sum of its parts.

important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! important! .

look here

Spa

ce mak

es gro

ups.

Spa

ce mak

es gro

ups.

Spa

ce mak

es gro

ups.

layered u

v v

Genome Res. 2018. 28: 357-366.

INDUCED

Nuc Ntz1 SAGA Hsf1 TFIIB TFIIH FACT Pol II Ser7p Ser5p Ser2p PIP-seq â&#x20AC;&#x201C;1kb

Genome Res. 2018. 28: 357-366.

1kb

REPRESSED

NO CHANGE

HSP24 mock

Genome Res. 2018. 28: 357-366.

heat shock

RPL3

REB1

Loucks et al., eLife (2019) 8:e37271

CILIATED DOPAMINERGIC NEURON tyrosine

mechanosensation

)))

POSTSYNAPTIC NEURON

DAT-1

DOP-1

tap habituation basal slowing response

DOP-3

swimming-induced paralysis avoidance

DOP-4

avoidance

CAT-2 K+ TRP-4

Na+ Ca2+

dopamine signal propagation Ca2+ UNC-2

CILIUM

SYNAPSE

CILIATED DOPAMINERGIC NEURON DAT-1

tyrosine

mechanosensation

)))

POSTSYNAPTIC NEURON

DOP-1

tap habituation basal slowing response

DOP-3

swimming-induced paralysis avoidance

DOP-4

avoidance

CAT-2 K+ Na+ Ca2+

TRP-4

dopamine signal propagation Ca2+ UNC-2

CILIUM

SYNAPSE

CILIATED DOPAMINERGIC NEURON tyrosine

mechanosensation

)))

POSTSYNAPTIC NEURON

DAT-1

DOP-1

tap habituation basal slowing response

DOP-3

swimming-induced paralysis avoidance

DOP-4

avoidance

CAT-2 K+ TRP-4

Na+ Ca2+

dopamine signal propagation Ca2+ UNC-2

CILIUM

SYNAPSE

CILIATED DOPAMINERGIC NEURON tyrosine

mechanosensation

)))

POSTSYNAPTIC NEURON

DAT-1

DOP-1

tap habituation basal slowing response

DOP-3

swimming-induced paralysis avoidance

DOP-4

avoidance

CAT-2 K+ TRP-4

Na+ Ca2+

dopamine signal propagation Ca2+ UNC-2

CILIUM

SYNAPSE

Ti Crystals

ECM PM Cytoplasm NE 1 First Contact

Lamins

Condensed Chromatin

2 “Outside-In” Signal Transduction

ItgB

Collagen Caveolae

PRC PcG

Upregulated Genes Ago3 B3Galt2 Omd

Omd

Ribosomes

Cav1

Rebbeca Reiss

B3Galt2

Downregulated Genes VegfA Cav1

Open Chromatin

Golgi

Glycosyl group

3 Chromatin Remodeling

LINC

ItgA

Nucleus

RISC Ago3

5 “Inside-Out” Signal Transduction

4 RNA Processing & Transport

FIRST CONTACT

OUTSIDE-IN SIGNAL TRANSDUCTION

CHROMATIN REMODELLING

INSIDE-OUT SIGNAL TRANSDUCTION

RNA PROCESSING AND TRANSPORT

FIRST FIRST CONTACT CONTACT ECM

2 OUTSIDE-IN

OUTSIDE-IN SIGNAL SIGNAL TRANSDUCTION TRANSDUCTION PM

CYTOPLASM

CHROMATIN

CHROMATIN REMODELLING REMODELLING

NM NM

NUCLEUS

lamins Ti Crystal

PcG

PRC

collagen LTGA LTGB

Chromatin FA

– VEGFA – CAV1

LINC

caveola

+ OMD + AGO3 + B3GALT2

closed

open

NP OMD

glycosyl group CAV1

RISC

INSIDE-OUT RNA PROCESSING SIGNAL AND TRANSPORT AGO3 B3GALT2 TRANSDUCTION

5 INSIDE-OUT SIGNAL TRANSDUCTION

4 RNA PROCESSING AND TRANSPORT

4 – downregulated + upregulated

Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad LOREM IPSUM Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet

Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

FIRSTFIRST CONTACT CONTACT ECM

Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

ECM

OUTSIDE-IN OUTSIDE-IN SIGNAL SIGNAL TRANSDUCTION TRANSDUCTION PM

CYTOPLASM CYTOPLASM

CHROMATIN

CHROMATIN REMODELLING REMODELLING

NUCLEUS

lamins

Ti Crystal

lamins PcG

Ti Crystal

LTGA LTGB

LTGA LTGB caveola

PRC

PcG

collagen

PRC

– VEGFA – CAV1 –

LINC

–

Chromatin

VEGFA closed

+ OMD CAV1 + AGO3 + B3GALT2 + OMD

caveola

closed open

+ AGO3 + B3GALT2

NP OMD

Chromatin

open

RISC

NP glycosyl group

B3GALT2

OMD

RISC

CAV1

glycosyl group CAV1

LOREM IPSUM Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad minim

AGO3

INSIDE-OUT RNA PROCESSING SIGNAL AGO3AND TRANSPORT B3GALT2 TRANSDUCTION

4 – downregulated

INSIDE-OUT SIGNAL TRANSDUCTION

5 Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

+ upregulated

RNA PROCESSING AND TRANSPORT

4 Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

– downregulated + upregulated

Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

FIRST CONTACT

OUTSIDE-IN SIGNAL TRANSDUCTION

CHROMATIN REMODELLING

ECM

CYTOPLASM

NUCLEUS

lamins Ti Crystal

PcG

PRC

collagen LTGA LTGB

Chromatin FA

– VEGFA – CAV1

LINC

caveola

+ OMD + AGO3 + B3GALT2

closed

open

NP OMD

glycosyl group

B3GALT2

RISC

AGO3

CAV1

LOREM IPSUM Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad minim

INSIDE-OUT SIGNAL TRANSDUCTION

5 Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

RNA PROCESSING AND TRANSPORT

4 Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

– downregulated + upregulated

Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

FIRST CONTACT

OUTSIDE-IN SIGNAL TRANSDUCTION

CHROMATIN REMODELLING

ECM

CYTOPLASM

NUCLEUS

lamins Ti Crystal

PcG

PRC

collagen LTGA LTGB

Chromatin – VEGFA – CAV1

LINC

caveola

+ OMD + AGO3 + B3GALT2

glycosyl group

B3GALT2

+ upregulated

RISC

AGO3

CAV1

LOREM IPSUM Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad minim

INSIDE-OUT SIGNAL TRANSDUCTION

5 Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

open

– downregulated

NP OMD

closed

RNA PROCESSING AND TRANSPORT

4 Lorem ipsum dolor sit amet, consectetuer adipiscing elit, sed diam nonummy nibh euismod tincidunt ut laoreet dolore magna aliquam erat volutpat. Ut wisi enim ad

J. Neurosci (2015) 35:11281â&#x20AC;&#x201C;11291.

IL-4 M2-MΘ M1-MΦ CD68-MΦ 0

time (days)

J. Neurosci (2015) 35:11281–11291.

IL-4 M2-MΘ M1-MΦ CD68-MΦ 1

J. Neurosci (2015) 35:11281–11291.

10 11

days

IL-4 M2-MΘ M1-MΦ CD68-MΦ 1

J. Neurosci (2015) 35:11281–11291.

10 11

days

rearrange elements to find patterns and trends

Diatoxanthin

Alloxanthin

PheophytinB

LuteinZeaxanthin 300

150

200

125 60

100

nmol pigment g 1 organic matter

100 30

0 Canthaxanthin

Aphanizophyll

Echinenone

PheophytinA

150 120

100 30 80 5

50 40

0 1940

1960

1980

2000

0 1940

1960

1980

2000

1940

1960

1980

2000

1940

1960

1980

2000

Year

Figure 4. Concentrations of select fossil pigments throughout time in sediments from Pelican Lake. Pigment concentration was determined by HPLC analysis.

2000

Alloxanthin

Echinenone

LuteinZeaxanthin

Canthaxanthin

PheophytinA

Diatoxanthin

PheophytinB

Aphanizophyll

Echinenone

LuteinZeaxanthin

Canthaxanthin

PheophytinA

Diatoxanthin

PheophytinB

Aphanizophyll

2000

Alloxanthin

Journal of Neuroscience (2016) 5128-5143.

CNP-cre

TNFR2

CNP-cre:TNFR2

CNP-cre

TNFR2

CNP-cre:TNFR2

Journal of Neuroscience (2016) 5128-5143.

TNFR1

TNF

IL1b

INFg

120

100

MBP

CXCL10

GPR17

PLP

120

100

Journal of Neuroscience (2016) 5128-5143.

TNFR1

TNF

IL1b

INFg

120

100

MBP

CXCL10

GPR17

PLP

120

100

TNF

INFg

IL1b

TNFR1

GPR17

MBP

PLP

CXCL10

120

100

Journal of Neuroscience (2016) 5128-5143.

use color responsibly

. !49

MOBA, museumofbadart.com

TITLE

. !50

MOBA, museumofbadart.com

TITLE

typical network analysis pipeline

FOXP2 CDH8 CDH5

typical network analysis pipeline

annotation with seed list

BIOLOGICAL NETWORK

FOXP2 FOXP2 CDH8 CDH8 CDH5 CDH5

clustering genes

identify candidate genes

typical network analysis pipeline

annotation with seed list

BIOLOGICAL NETWORK gene co-expression protein-protein interaction

clustering genes

identify candidate genes

FOXP2 FOXP2 CDH8 CDH8 CDH5 CDH5

association with particular phenotype or otherwise of interest

based on pathways, functional annotation (KEGG) or other clustering methods

derived from clusters containing genes from seed list

Wong, B. (2011) Points of View: Points of Review II. Nat Meth 8:189.

BREWER PALETTES

QUALITATIVE

SEQUENTIAL

DIVERGING

set1

blues

spectral

set2

greens

rdylbu

pastel2

reds

rdylgn

dark2

ylorbr

piyg

www.colorbrewer.org & mkweb.bcgsc.ca/brewer

www.co lo r brewer.org

colorbrewer.org

Satellite stem

Committed satellite stem

commitment

Myoblast

activation

Myocyte

early differentiation

Myotube

late differentiation

Satellite stem

Committed satellite stem

commitment

Myoblast

activation

Myocyte

early differentiation

Myotube

late differentiation

Pax7 Myf5 MyoD MyoG Mrf4 MyHC

Pax7 Myf5

MyoD MyoG Mrf4 MyHC

TITLE

. !62

% 40

100 80 60 MUTATIONS 40 20 H

APOBEC SIGNATURE M L

HIV STATUS

PIK3CA

PIK3CA 35 FAT1 19

FAT1

MLL2 15

MLL2

FBXW7 10

FBXW7

CASP8 7

CASP8 SLC35G5

SLC35G5 7

MAPK1

MAPK1 5

PCDHGA12

PCDHGA12 5 PSPC1 5

PSPC1

ZNF750 4

ZNF750

PCDHA9 3

PCDHA9 ZC3H6

ZC3H6 3 HRD AGE AT DIAGNOSIS CANCER STAGE HISTOLOGY

MUTATIONS

COPY NUMBER

HISTOLOGY

HRD

AGE GROUP

CANCER STAGE

synonymous

amplification

squamous

<10

<45

non-synonymous

deletion

adenosquamous

10–30

45–64

start gained

adeno

>30

>65

III

stop gained

neuroendocrine

frameshift multi-hit

IV unknown

unknown

mkweb.bcgsc.ca/colorblind

poster hospital

â&#x2014;?

â&#x2014;? no patient has ever died

Role of saltbush on free range layer farms Carolyn de Koning1 and Mini Singh2

Introduction

Results

Oldman saltbush (Atriplex nummularia) has potential to be used on free range poultry farms for shelter and shade. Saltbush contains anti nutritive factors and is high in NaCl. It is important to determine if there are negative or positive effects for hens that may eat saltbush.

Objective 1: • Layer hens do eat saltbush (Figure 1). • An estimated 5% of their dietary dry matter intake was saltbush.

• Objective 2: Does the consumption of saltbush by hens affect their production, welfare and product quality?

Methods Objective 1: Hy-Line Brown layers from 16 weeks to 27 weeks were given access to fresh saltbush on the outdoor range. Alkane analysis was used to estimate the amount of saltbush eaten by the hens. Objective 2: Air-dried saltbush was mixed to dilute layer crumbles at 0%, 5%, 10%, 15% and 20%. Fifteen individually housed Hy-line Brown hens per treatment were fed the diets for 28 days (32–35 weeks old).

Objective 2: • Saltbush in the diet had no impact on egg production, hen live-weight and feed intake. • Moisture content of hen excreta significantly increased with saltbush in the diet (Figure 2). • Egg quality was unaffected, except high saltbush eggs had stronger egg yolk colour compared to control eggs (Figure 3). • Consumer tests showed higher preferences for high saltbush eggs. a

% moisture in excreta

• Objective 1: Determine if free range laying hens eat saltbush

81.73

b b

77.25

78.55

79.97

73.69

10%

15%

20%

% saltbush fed in diet Figure 2: Average percentage moisture in the excreta from hens at peak lay fed air dried saltbush at 0%, 5%, 10%, 15% and 20% in a commercial layer diet. Different superscript letters show significant diet effects at P<0.001

Figure 3: Yolk colour of hard boiled eggs from hens fed saltbush at 0% (left image) and 20% (right image). Statistically significant diet effects at P= 0.0057 for yolk colour (Roche fan) from uncooked eggs.

Conclusions • Saltbush can be used to provide shade and shelter. • Feeding saltbush enhanced yolk colour and consumers had a higher preference for high saltbush eggs. • Free range layer hens will not eat enough fresh saltbush to impact their production. Figure 1: Top image: Fresh saltbush provided on the outdoor range. Bottom image: Hens had stripped and eaten the leaves of saltbush within three days.

ACKNOWLEDGEMENTS

CONTACTS

We thank Poultry CRC for providing funds for this project.

1 South Australian Research and Development Institute (SARDI), Roseworthy Campus,, South Australia, 5371; Carolyn.dekoning@sa.gov.au 2 School of Life and Environmental Sciences, The University of Sydney, Camden, NSW 2570, Australia

SALTBUSH: Comfortable hens, colorful yolks. Carolyn de Koning, Mini Singh WHY SALTBUSH?

SALTBUSH AS A NUTRIENT SOURCE

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit suscipit eros in viverra. Donec interdum, quam quis egestas cursus, risus libero maximus lorem, id consectetur risus nunc eget risus. Nulla felis ante, tristique vitae tellus id, fringilla rhoncus sem. Suspendisse pretium lectus vel magna euismod, non ornare tortor tempor. Sed et leo vulputate, auctor ipsum quis, tincidunt nisi. Donec quis erat nec diam rutrum mollis. Sed nec euismod ante. Integer accumsan tortor id quam aliquam viverra.

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit suscipit eros

METHODS

FIGURE 1 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla

A SALTBUSH STRIPPED AND EATEN BY HENS WITHIN 3 DAYS

% MOISTURE IN EXCRETA

0 saltbush 5 in diet 10 15 (%) 20

73.7 a

80 77.2 b 78.6 b 80.0 bc

81.7

% moisture in excreta

0 10 20 saltbush in diet (%) FIGURE 2 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla

BENEFITS OF SALTBUSH Saltbush improves hen welfare and comfort by providing shade, shelter and nutriets without impacting production. Consumers prefer the yolk color of eggs from hens that fed on saltbush.

SALTBUSH ENHANCES YOLK COLOR Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit suscipit eros CONSUMERS PREFERRED SALTBUSH EGGS

ACKNOWLEDGEMENTS

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit suscipit eros

FIGURE 2 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla

[1] Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. [2] Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit suscipit eros in viverra. Donec interdum, quam quis egestasaugue. Fusce

Not hungry? A case report of feed refusal of laying hens I Ruhnke1, C Normant1,2, Z Iqbal1, DLM Campbell1,3, J Zentek4 and M Choct5 1Animal Science, School of Environmental and Rural Science, University of New England, Armidale NSW 2351, Australia 2Institut Polytechnique LaSalle Beauvais, Beauvais, France 3CSIRO, Agriculture and Food, Armidale NSW 2350, Australia 4Institute of Animal Nutrition, Freie Universität Berlin, Germany 5Poultry Cooperative Research Centre, University of New England, Armidale NSW 2351, Australia

APPETITE OR AESTHETIC? Feed intake of laying hens can be affected by a variety of factors. Physical presentation of the feed (e.g. colour, particle size, smell) is known to affect feed selection. Sudden changes of the physical feed presentation (for example mash feed to pelleted feed), or the level of feed de-mixing have been reported to reduce feed acceptance. A reduced hygienic status of feed due to bacterial or mycotoxin contamination can result in a limited voluntarily feed intake. CONTROL 120

100

15 10

100

5 60

0 0

Despite physical and chemical testing of the feed, the reason for the feed refusal remains unknown.

LAYING PERFORMANCE

TOTAL 120

Feed refusal due to reduced health status was not a factor.

BODY WEIGHT

FEED CR

FEED INTAKE CHOICE

KEY DISCOVERIES Hens showed no clinical symptoms of a disease and appeared healthy and active.

2.1

100

2.0

EGG MASS

1.9 2

EGG WEIGHT 60 50

1.8

30 40

week 3

20 0

CONTROL

−5

TREATMENT % DIFFERENCE

−10

0 −10

MYCOTOXIN LEVELS aflatoxin B1, B2, G1, G2 ochratoxin A deoynivaleol nivalenol HT2 toxin T2 patulin

< 0.001 < 0.001 < 0.05 < 0.05 < 0.05 < 0.05 < 0.05

NEW FEED

< 0.001 < 0.001 < 0.05 < 0.05 < 0.05 < 0.05 < 0.05

NUTRIENT CONTENT crude protein histidine serine arginine glycine aspartic acid glutamic acid threonine alaninie proline lysine tyrosine methionine valine isoleucine leucine phenylalanine ether extract calcium phosphorous sodium

183.6 4.6 9.4 12.0 8.7 16.6 41.5 6.8 7.7 13.0 9.2 4.5 3.8 9.2 7.8 13.8 9.2 32.4 44.8 0.5 21.9

162.3 4.8 9.9 12.6 9.1 17.8 42.9 7.2 8.1 13.3 9.8 4.7 3.7 9.7 8.2 14.5 9.7 25.6 41.3 0.4 19.4

30 20

−20

FIGURE 1 | Weekly performance of control and choice feed treatment groups.

REFUSED FEED

−10

−20

FEED ASSAY

−5

−15

TABLE 1 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. TABLE 2 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu mo% DIFFERENCE

-11.6 4.3 5.3 5.0 4.6 7.2 3.4 5.9 5.2 2.3 6.5 4.4 -2.6 5.4 5.1 5.1 5.4 -21.0 -7.8 -14.0 -11.4

–5 0 +5

METHODS

FEED MIX SCHEDULE WEEK 1 2 3 4 5

CONTROL n = 4 × 20

TREATMENT n = 4 × 20

+ dried soldier fly larvae

160 ISA brown free-range laying hens (20 hens/pen). All hens received ad lib a typical Australian wheat-soy based layer mash formulated according to the breed recommendations. Control group: hens of 4 pens were housed under standard conditions. Treatment group: hens of 4 pens housed under standard conditions and received in addition to the standard diet ad lib dried Black Soldier Fly (Hermetia illucens) larvae (BSF). The standard layer diet was mixed on two different time points (one month apart) by the same people from the same batch of ingredients. Mix 1 was fed during the adaptation period when hens were 38 - 43 weeks of age. Feed intake during this adaptation period was ~ 116 g/hen/day. Feed was switched from mix 1 to mix 2 with the beginning of the choice feeding (Week 1, Table 1). Feed intake decreased dramatically for the control and choice fed groups, respectively. Laying performance, egg weight, egg mass, and body weight decreased dramatically with lowest levels observed in Week 4. After changing the diet to a newly mixed batch (mix 3), feed intake and production data recovered. RESULTS Physical evaluation of feed quality was performed by sensory testing. The refused feed was dry, aromatic without foreign odours, was of product typical colour, homogenous, and free from macroscopic contamination such as mould, mites, etc. Dry matter (% w/w) was 89.8% for the refused feed (mix 2) and 91.5% for the new mixed feed (mix 3). The feed was evaluated for mycotoxins, and results are displayed in Table 2. In order to exclude a mixing error or de-mixing of the feed, chemical feed analysis of macro and micro ingredients was performed. Results are displayed in Table 3.

FEED INTAKE CHOICE

CONTROL 120

100

15 10

100

5 60

0 0

Feed refusal due to reduced health status was not a factor. Despite physical and chemical testing of the feed, the reason for the feed refusal remains unknown.

BODY WEIGHT

LAYING PERFORMANCE

TOTAL 120

KEY DISCOVERIES Hens showed no clinical symptoms of a disease and appeared healthy and active.

2.1

100

2.0

1.9 2

EGG WEIGHT

EGG MASS 60 50 40

1.8

30 40

week 3

CONTROL

−5

TREATMENT % DIFFERENCE

−10 −15

10 0

−5 −10 −15

−10

−20

FIGURE 1 | Weekly performance of control and choice feed treatment groups.

2 0

METHODS

10 0

Ascaridia galli infection lowers egg production and mass but not quality N Sharma1, P Hunt2, B Hine2, RA Swick1, C Normant1,3 NK Sharma1, Z Iqbal1, I Ruhnke1 1School of Environmental and Rural Science, University of New England, Armidale NSW 2351, Australia 2CSIRO, McMaster Laboratory, Chiswick, Armidale NSW 2350, Australia 3Institut Polytechnique LaSalle Beauvais, Beauvais, France

THE MOST COMMON GI PARASITE Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit suscipit eros in viverra. Donec interdum, quam quis egestas cursus, risus libero maximus lorem, id consectetur risus nunc eget risus. Nulla felis ante, tristique vitae tellus id, fringilla rhoncus sem. Suspendisse pretium lectus vel magna euismod, non ornare tortor tempor. Sed et leo vulputate, auctor ipsum quis, tincidunt nisi. Donec quis erat nec

FIGURE 1 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci conval-

FIGURE 2 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean

THE EXPERIMENT 4 A. GALLI INFECTION LEVELS

5 REPLICATE PENS

× 10

10 10 10 Lohmann hens

–

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a,

MEASUREMENTS feed intake

250 1,000 2,500 eggs

4,000

EGG WEIGHT (g)

WEEK 20 No effect

No effect

8,000

LMH

–

30, 40 week

EGG MASS (g)

PRODUCTION (%)

Effect at low infection level b

100

2,000 0

–

egg quality

IMPACT ON EGG QUALITY AND PRODUCTION

A. GALLII WORM COUNT

WEEK 20 No effect

egg weight

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit sus-

TRACKING THE INFECTION

WEEK 8–20 Peak at week 11

egg production

25, 30, 35, 40 week

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a,

EXCRETA EGG COUNT

body weight

FIGURE 3 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit suscipit eros in viverra. Donec interdum, quam quis egestas cursus, risus libero maximus lorem, id consectetur risus nunc eget risus. Nulla felis ante, tristique vitae tellus id, fringilla

–

Significant reduction in egg mass and production at low infection level. 70 M H – L M H

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This project (project number 1.5.9) was funded by the Poultry CRC established and supported under the Australian Government’s Cooperative Research Centres Program. Travel to this conference and subsequently poster presentation was sponsored by the Australian Egg Corporation Ltd.

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FIGURE 2 | Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean

THE EXPERIMENT 4 A. GALLI INFECTION LEVELS

5 REPLICATE PENS

Ă&#x2014; 10

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250 1,000 2,500 eggs

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MEASUREMENTS feed intake

body weight

egg production

25, 30, 35, 40 week

egg weight

egg quality 30, 40 week

Lorem ipsum dolor sit amet, consectetur adipiscing elit. Quisque a orci convallis, sollicitudin risus a, eleifend magna. Nulla facilisi. Aenean eu molestie risus. Fusce hendrerit sus-

Alpha synuclein overexpression alters epigenetic regulation of neurodevelopmental and metabolic pathways in dopaminergic neurons Schaffner, S. L.1,2, Lazaro, D.3, Paiva, I.3, Outeiro, T. F.3,4,5, & Kobor, M. S.1,2,6 for Molecular Medicine and Therapeutics, BC Children’s Hospital, Vancouver, BC, Canada; 2Dept. of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada; 3Department of Experimental Neurodegeneration, Center for Nanoscale Microscopy and Molecular Physiology of the Brain, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Goettingen, 37073, Goettingen, Germany 4CEDOC – Chronic Diseases Research Center, Faculdade de Ciencias Medicas, Universidade Nova de Lisboa, Lisboa, Portugal 5Max Planck Institute for Experimental Medicine, 37075 Goettingen, Germany 6Human Early Learning Partnership, University of British Columbia, Vancouver, BC, Canada 1Centre

In this study, we investigated the effects of SNCA overexpression and mutation on two epigenetic marks – DNA methylation and DNA hydroxymethylation – in a dopaminergic neuron tissue culture system, using the Illumina EPIC BeadChip Array. We found that wild-type and A30P mutant SNCA had many similar effects on the DNA methylome of dopaminergic neurons. However, each SNCA genotype also had distinct effects on the epigenome; the wild type protein altered DNA methylation at more CpG sites overall, found in neurodevelopmental and synaptic function genes, while the A30P mutant altered DNA methylation and hydroxymethylation at CpG sites found in genes regulating glucose metabolism.

3.1. Results: Both SNCA-OE and A30P cells were differentially methylated at genes involved in motor function. D

1. Introduction

A-B) Volcano plots showing results of linear modeling (DNAhm ~ Genotype) in control vs SNCA-OE or A30P cells; red = sites with decreased DNAm at FDR <= 0.05 and absolute delta beta >= 0.05; grey = non-significant sites; blue = sites with decreased DNAm at FDR <= 0.05 and absolute delta beta >= 0.05. C) Venn diagram showing the number of differentially hydroxymethylated sites unique to each genotype and shared between genotypes. D) Heatmap showing beta values at the 37 CpG sites that were differentially hydroxymethylated in A30P cells only; red = low DNAm, blue = high DNAm. E) Top three CpG sites that were differentially hydroxymethylated in A30P cells only, ranked by delta beta. F) Result of gene ontology enrichment analysis on the 37 CpG sites differentially hydroxymethylated in A30P cells only at p < 0.01.

3.5. Results: DNA methylation and hydroxymethylation may contribute to transcriptional deregulation of a glutamate signaling network in both SNCAOE and A30P cells. A NS

expression

NoData N D Up

0 1.39>5.99 edge C24 D

Wang et al., Front Mol Neurosci 2016

• SNCA mutation/multiplication alone doesn’t always lead to familial PD; and SNCA SNPs also contribute to sporadic PD2 • The epigenome may mediate PD genetic risk from SNCA and environmental risk from lifestyle, nutrition, and toxic exposures3-6 • DNA methylation and DNA hydroxymethylation are two stable, easily measurable epigenetic marks in brain tissue which may influence gene expression7-8

A) Heatmap showing beta values at a sample of 100 CpG sites that were differentially methylated in SNCA-OE cells only; red = low DNAm, blue = high DNAm. B) Top three CpG sites that were differentially methylated in SNCA-OE cells only, ranked by delta beta. C) Result of gene ontology enrichment analysis on the 2428 CpG sites differentially methylated in SNCA-OE cells only at p < 0.01.

A) Heatmap showing beta values at the 24 CpG sites that were differentially methylated in A30P cells only; red = low DNAm, blue = high DNAm. B) Top three CpG sites that were differentially methylated in A30P cells only, ranked by delta beta. C) Result of gene ontology enrichment analysis on the 24 CpG sites differentially methylated in A30P cells only at p < 0.01.

Williams et al., EMBO Reports 2012

Lill, Mol Cell Probes 2016

OpenSea/Body SNCA-OE DB -0.08 SNCA-OE FDR 0.04

DLG4

DNAm hits (FDR <= 0.01, DB >= 0.1)

GRIK1 CpG island/TSS200 SNCA-OE DB -0.102 SNCA-OE FDR 1.87e-7

GRIK2 DLG3

CpG island/TSS200 SNCA-OE DB -0.135 SNCA-OE FDR 2.45e-7

Paiva et al., Hum Mol Genet 2017

A30P DB -0.05 A30P FDR 0.03

GRIK4

DLG1

CpG island/TSS200 SNCA-OE DB -0.102 SNCA-OE FDR 1.54e-6

OpenSea/Body SNCA-OE DB 0.139 SNCA-OE FDR 1.76e-7

GRIK5

A) Regulatory protein-protein interaction module generated using DNA methylation, DNA hydroxymethylation, and gene expression changes between control and SNCAOE cells. B) Differentially hydroxymethylated CpG site within the GRIK2 gene. C) Differentially methylated CpG sites within the GRIK2 gene. D) GRIK2 expression fold change in control, SNCA-OE, and A30P cells.

Conclusions •

•

• •

3.3. Results: A30P cells were differentially methylated at genes involved in glucose metabolism.

GRIK3

NCALD

A-B) Volcano plots showing results of linear modeling (DNAm ~ Genotype) in control vs SNCA-OE or A30P cells; red = sites with decreased DNAm at FDR <= 0.01 and absolute delta beta >= 0.1; grey = non-significant sites; blue = sites with decreased DNAm at FDR <= 0.01 and absolute delta beta >= 0.1. C) Venn diagram showing the number of differentially methylated sites unique to each genotype and shared between genotypes. D) Heatmap showing beta values at the 129 CpG sites that were differentially methylated in both genotypes; red = low DNAm, blue = high DNAm. E) Top three CpG sites that were differentially methylated in both genotypes, ranked by delta beta. F) Result of gene ontology enrichment analysis on the 129 CpG sites differentially methylated in both genotypes at p < 0.01.

Glutamate receptor

hydroxy promoter

Guanylate cyclase; NMDA receptor clustering at synapses

3.2. Results: SNCA-OE cells were differentially methylated at genes involved in neurodevelopment and synaptic function.

hydroxy body

methylation enhancer

Kara et al., Neurosci Letters 2013

DNAhm hit (FDR <= 0.05, DB => 0.05)

0.02 5.37>9.49

methylation body

Network built around GRIK2 Chi−square P−value= 0

hydroxy enhancer

N D N

methylation promoter

Down N

node C2

• Under pathological conditions or when overexpressed, SNCA can form oligomers, fibrils, and aggregates, impairing function1 • The A30P missense mutation disrupts the ability of SNCA to bind membranes1

N D N

These results suggest that there are some epigenetic pathways that may be commonly dysregulated among those with different SNCA variants, and some that are unique. This may help in understanding why PD manifests differently across individuals, and encourages stratification by SNCA genotype for further research.

The alpha synuclein (SNCA) gene encodes a protein that is found at synaptic terminals and regulates neuronal differentiation, survival, and metabolism as well as SNARE complex assembly. Multiplications of SNCA and missense mutations are linked to familial Parkinson’s disease (PD). SNPs in SNCA may also contribute to development of sporadic PD. However, it is not fully understood why only some individuals with SNCA variants will develop disease, or what specific role SNCA SNPs play in sporadic PD. Environment and lifestyle likely modulate the probability that genetically at-risk individuals will develop PD, and the epigenome may mediate these genetic and environmental contributions to disease.

3.4. Results: A30P cells also had increased DNA hydroxymethylation at genes regulating glucose metabolism.

2. Methods

Abstract

A C

Overexpression of wild type and A30P mutant SNCA have many similar effects on the epigenome, and may induce epigenetic and transcriptional dysregulation of motor function pathways such as GRIK2-DLG3 glutaminergic signaling Overexpression of wild type SNCA induces differential DNA methylation at genes regulating neurodevelopment and synaptic function Overexpression of A30P SNCA induces differential DNA methylation and hydroxymethylation at genes regulating glucose metabolism Ability of wild type vs mutant SNCA to bind membranes and/or receptor targets may underlie differential effects of each genotype on DNA methylation

Acknowledgements Thank you to Julia MacIsaac, David Lin, and Katia Ramadori for running samples on the EPIC BeadChip. Thank you also to Rachel Edgar and David Lin for advice on analysis of DNA hydroxymethylation data. SLS was supported by a Faculty of Medicine Four Year Doctoral Fellowship. MSK is the Canada Research Chair in Social Epigenetics, Senior Fellow of the Canadian Institute for Advanced Research, and Sunny Hill BC Leadership Chair in Child Development. This work is conducted under a Transnational “Epigenomics of Complex Diseases” grant (CIHR EGM-141897, ANR-15-EPIG-0001, BMBF 01KU1503A).

References 1Wang,

C. et al. Fron Mol Neurosci 2016, 9:48. 2Lesage, S., & Brice, A. Hum Mol Genet 2009, R48-R59. 3Ascherio, A., & Schwarzchild, M. A. Lancet Neurol 2016, 14:1257-1272. 4Coppede, F. Sci World J 2012, 489830. 5Chuang, Y., et al. Genome Med 2017, 9:76. 6Wassouf, Z., et al. Front Cell Neurosci 2018, 12:112. 7Jones, P. A. Nat Rev Genet, 13: 484-492. 8Wen, L., Li, X., Yan, L. et al. Genome Biol 2014, 15(3):1-17.

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