Download (Japan), organized by Nori Satoh

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br
is
af
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W
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H
an
Limbs
Vertebrates
Jaws
Paired
appendages
Cephalochordates
Urochordates
Stem
chordates
Big brain
Neural crest
Placodes
Dorsal nerve cord
Notochord
Gill slits
Large-scale Gene
Duplications
“What characterizes the living world is both its diversity and its underlying unity”
PARADOX: “Phenotypic diversity versus genetic unity”
http://drujohnwigsinkiwi.files.wordpress.com/2007/01/fly2.jpg
http://en.wikipedia.org/wiki/Image:Mus_Musculus-huismuis.jpg
http://www.mun.ca/biology/desmid/brian/BIOL3530/DB_Ch15/figB4_A.jpg
Evolutionary Genomics allows us to test that paradox
• We have access to all genes present in the genome of an organism
• We also can also detect those genes that are missing
INVERSE PARADOX: “Genetic diversity versus phenotypic unity”
Chordates in context
Urochordates
Olfactores
Trait:
Chordates in context
Larvaceans Ascidians
Oikopleura Ciona
OLD
UROCHORDATES
(Tunicates)
Amphioxus
Zebrafish
CEPHALOCHORDATES
VERTEBRATES
?
NEW
Amphioxus
CEPHALOCHORDATES
Larvaceans Ascidians
Oikopleura Ciona
UROCHORDATES
(Tunicates)
Trait loss
Zebrafish
VERTEBRATES
Larvaceans retain chordate features as adults
Oikopleura larva
0.1 mm
Gill slits
Anus
Dorsal hollow nerve cord Notochord
Muscle blocksPost-anal Tail
Zebrafish larva
0.1 mm
absence of Midbrain in urochordates
Zebrafish
Oikopleura dioica Ciona intestinalis
FOREBRAIN
Oikopleura larva
HINDBRAIN
VERTEBRATES
UROCHORDATES
(Cañestro, Bassham and Postlethwait, 2005 Dev Biol)
FOREBRAIN
HINDBRAIN
SPINAL CORD
FOREBRAIN
MIDBRAIN
HINDBRAIN
Zebrafish larva
SPINAL CORD
Midbrain, vertebrate innovation or urochordate simplification?
Larvaceans Ascidians
Oikopleura Ciona
Amphioxus
CEPHALOCHORDATES
UROCHORDATES
(Tunicates)
Zebrafish
VERTEBRATES
Trait loss?
?
Trait: presence of midbrain
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
(Cañestro and Postlethwait, 2007 Dev Biol)
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
Retinoic acid (RA)
•RA is a derivative of vitamin A
•RA basic role is to inhibit cell proliferation, and to activate mechanisms of cell differentiation and
apoptosis.
•In humans, as in other vertebrates, RA plays important physiological roles:
Early embryogenesis (axial patterning), the formation of limbs, eyes
Respiratory system, nervous system, reproductive system, hematopoietic system
•Alterations in the RA metabolism or the pathways of RA action can lead to pathologic conditions
such as cancer, dermatologic diseases, osteoporosis, rheumatoid arthritis, and premature births.
•The broad range of RA functions has led to RA being targeted to develop applications, ranging from
the use of RA anti-proliferative properties in therapeutic treatments against cancer, to the use of antiaging properties of RA in the industry of the skin care.
•Therefore, the study of the synthesis of RA and the mechanisms of RA action is important not only
to better understand the physiological roles of the RA and develop new applications, but also to
prevent these applications from becoming toxic by altering the physiological levels of RA and posing a
risk for the human health.
Action of Retinoic Acid Genetic Machinery
Vitamin A
(Retinol)
(Raldh)
RARE
“Collinearity” of Hox-cluster gene expression:
•spatial
•temporal
http://www.mun.ca/biology/desmid/brian/BIOL3530/DB_Ch15/figB4_A.jpg
SPATIAL and TEMPORAL COLINEAR expression of Hox gene cluster
AP axis
RA regulates TEMPORAL COLINEAR expression of Hox gene cluster
Choreographed looping out of chromosome territories by RA-induced chromatin decondensation.
Transcription factors
Hoxb1
Hoxb9
RA
chromosome
RA
(Chambeyron and Bickmore, 2004)
SPATIAL and TEMPORAL COLINEAR expression of Hox gene cluster
AP axis
RA regulates TEMPORAL COLINEAR expression of Hox gene cluster
Choreographed looping out of chromosome territories by RA-induced chromatin decondensation.
1
Hoxb1
Transcription factors
Hoxb9
RA
chromosome
RA
(Chambeyron
(Chambeyron
and
and
Bickmore,
Bickmore,
2004)
2004)
SPATIAL and TEMPORAL COLINEAR expression of Hox gene cluster
AP axis
RA regulates TEMPORAL COLINEAR expression of Hox gene cluster
Choreographed looping out of chromosome territories by RA-induced chromatin decondensation.
1
Hoxb1
1
Hoxb9
RA
RA
Transcription factors
2
RA
Chromatin
structure
Genomic
architecture
chromosome
(Chambeyron and Bickmore, 2004)
RETINOIC
RETINOIC ACID
ACID crucial for AnteroPosterior CNS patterning in Chordates
RA-induced Homeotic transformation (POSTERIORIZATION)
Midbrain Hindbrain
Forebrain
Hindbrain
Fore/Midbrain
RA
RA
RA
(modified from Schilling and Knight, 2001)
CEPHALOCHORDATES
UROCHORDATES
(Ascidians)
VERTEBRATES
“Innovation” of RA-genetic
machinery was a milestone for the
origin of chordate bodyreviewed
plan.in Fujiwara (2006)
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
RA-genetic machinery
ALDH1A
CYP26
RAR
?
?
?
?
?
?
AMBULACRARIA
?
?
?
?
?
CHORDATES
Echinoderms Hemichordates Cephalochordates Urochordates
AscidiansLarvaceans
Vertebrates
1. RA-genetic machinery is NOT a chordate innovation
ALDH1A
CYP26
RAR
AMBULACRARIA
CHORDATES
Echinoderms Hemichordates Cephalochordates Urochordates
Vertebrates
AscidiansLarvaceans
+
(Cañestro, Postlethwait, Gonzalez-Duarte, Albalat 2006 Evo Dev)
2. RA genetic machinery have been lost in Oikopleura
ALDH1A
CYP26
RAR
AMBULACRARIA
CHORDATES
Echinoderms Hemichordates Cephalochordates Urochordates
Vertebrates
AscidiansLarvaceans
ALDH2
prediction:
ALDH1A1/2/3
AP axial patterning
in Oikopleura is independent of RA
“ALDH2”
(Cañestro, Postlethwait, Gonzalez-Duarte, Albalat 2006 Evo Dev)
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
Endogenous β-galactosidase activity
Amphioxus
(Cañestro et al., 2001)
Oikopleura
DMSO
*
Figure 3
DMSO
*
Pharynx
Posterior gut
10-6 M RA
Pharynx
Homeotic
posteriorization
10-6 M RA
RA does NOT cause homeotic posteriorization in Oikopleura
Hox1
Pax2/5/8a
RA
DMSO
Otx
Figure 4
Figure 5
Figure 6
AP axial patterning in Oikopleura is independent of RA
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
• “genetic diversity”: In contrast to Oikopleura, Ascidians have a full RA-genetic machinery
•“phenotypic unity”: Oikopleura and ascidians share a basic AP axial patterning
Hox1
CNS
Ciona
Hox1
Epidermis
(Nagatomo & Fujiwara, 2003)
CNS Oikopleura
Epidermis
(Cañestro et al., 2005)
Evo-Devo “inverse paradox”:
“similar morphology” despite “different genetic machinery”
(Cañestro, Yokoi and Postlethwait, 2007 Nature Reviews Genetics)
Ascidians
palp cells
HrETR-1
DMSO
DMSO
RA
HcPax2/5/8
RA
DMSO
RA
HrHox1
RA posteriorization
RA
DMSO
(Katsuyama et al., 1995)
(Katsuyama et al., 1995, 1998)
“Shortened head”
or “Moonfaced”
(Yagui and Makabe, 2002)
RA affects palp morphogenesis
(Hinman and Degnan, 2000)
NO posteriorization
In agreement with our results in Oikopleura, RA does NOT seem to
AP axial patterning became independent of RA in stem urochordate
induce homeotic posteriorization in ascidians.
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
Abstract
Developmental signaling by retinoic acid (RA) is thought to be an innovation essential
for the origin of the chordate body plan. The larvacean urochordate Oikopleura dioica
maintains a chordate body plan throughout life, and yet its genome appears to lack
genes for RA synthesis, degradation, and reception. This suggests the hypothesis that
the RA-machinery was lost during larvacean evolution, and predicts that Oikopleura
development has become independent of RA-signaling. This prediction raises the
problem that the anterior–posterior organization of a chordate body plan can be
developed without the classical morphogenetic role of RA. To address this problem, we
performed pharmacological treatments and analyses of developmental molecular markers
to investigate whether RA acts in anterior–posterior axial patterning in Oikopleura
embryos. Results revealed that RA does not cause homeotic posteriorization in
Oikopleura as it does in vertebrates and cephalochordates, and showed that a chordate can
develop the phylotypic body plan in the absence of the classical morphogenetic role of RA.
A comparison of Oikopleura and ascidian evidence suggests that the lack of RA-induced
homeotic posteriorization is a shared derived feature of urochordates. We discuss
possible relationships of altered roles of RA in urochordate development to genomic
events, such as rupture of the Hox-cluster, in the context of a new understanding of
chordate phylogeny.
Conclusions
Trait: AP axial patterning is dependent of RA
“Genetic variability” vs
“Phenotypic unity”
Cephalochordates
Urochordates
Ascidians
Vertebrates
Larvaceans
Loss of RA-machinery
Trait loss: AP axial patterning independent of RA
Conclusions
(Ikuta et al. 2004)
1 2 3 4 5 6 7 8 9 1011121314
Cephalochordates
1
2-4
10 6-5
1213
(Seo et al. 2004)
1 2
4
9 9’10111213
Urochordates
Ascidians
1 2 3 4 5 6 7 8 9 10111213
A
B
C
D
Hox gene
organization
Vertebrates
Larvaceans
Loss of RA-machinery
1.AP axial patterning independent of RA
2.Hox-cluster rupture & Loss of temporal collinearity
Conclusions
(Ikuta et al. 2004)
1 2 3 4 5 6 7 8 9 1011121314
Cephalochordates
1
2-4
10 6-5
1 2
4
9 9’10111213
Urochordates
Ascidians
Oikopleura
no temporal colinearity
1213
(Seo et al. 2004)
1 2 3 4 5 6 7 8 9 10111213
A
B
C
D
Hox gene
organization
Vertebrates
Larvaceans
Loss of RA-machinery
1.AP axial patterning independent of RA
2.Hox-cluster rupture & Loss of temporal collinearity
Conclusions
1 2 3 4 5 6 7 8 9 1011121314
Cephalochordates
1
2-4
10 6-5
1213
1 2
4
9 9’10111213
Urochordates
Ascidians
1 2 3 4 5 6 7 8 9 10111213
A
B
C
D
Vertebrates
Larvaceans
Loss of RA-machinery
1.AP axial patterning independent of RA
2.Hox-cluster rupture & Loss of temporal collinearity
3.Genome diminution (e.g. Gbx loss)
Urochordate Determinative development/ rapid embryogenesis
Conclusions
1 2 3 4 5 6 7 8 9 1011121314
Cephalochordates
1
2-4
10 6-5
1213
1 2
4
9 9’10111213
Urochordates
Ascidians
1 2 3 4 5 6 7 8 9 10111213
A
B
C
D
Vertebrates
Larvaceans
Loss of RA-machinery
1.AP axial patterning independent of RA
2.Hox-cluster rupture & Loss of temporal collinearity
3.Genome diminution (e.g. Gbx loss)
So ... now, what do you think?
Is the midbrain a vertebrate innovation?
or maybe a urochordate simplification?