Somitogenesis

Embryology - 5 Dec 2023        Expand to Translate
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Introduction

Human embryo (week 4, Carnegie stage 11) Somites

The term somitogenesis is used to describe the process of segmentation of the paraxial mesoderm within the trilaminar embryo body to form pairs of somites, or balls of mesoderm. In humans, the first somite pair appears at day 20 and adds caudally at 1 somite pair/90 minutes until on average 44 pairs eventually form.

A somite is added either side of the notochord (axial mesoderm) to form a somite pair. The segmentation does not occur in the head region, and begins cranially (head end) and extends caudally (tailward) adding a somite pair at regular time intervals. The process is sequential and therefore used to stage the age of many different species embryos based upon the number visible somite pairs.

A mesenchymal to epithelial transition defines the outer cellular "shell" of the developing somite, with the core cells remain as a mesenchymal organisation. During early somite development a transient fluid-filled space, the somitocoel, can be identified in each somite and is later lost by cell proliferation. Neural crest cells later also enter and mix with the somatic cells.

Somites give rise to many different connective tissues including: cartilage, bone, muscle and tendon.

Cranial paraxial mesoderm remains unsegmented, and does not form somites, and will form the pharyngeal muscle progenitor field, the embryonic origin of facial and neck muscles.

Some Recent Findings

Mouse somitogenesis genes

In vitro characterization of the human segmentation clock "The segmental organization of the vertebral column is established early in embryogenesis, when pairs of somites are rhythmically produced by the presomitic mesoderm (PSM). The tempo of somite formation is controlled by a molecular oscillator known as the segmentation clock1,2. Although this oscillator has been well-characterized in model organisms1,2, whether a similar oscillator exists in humans remains unknown. Genetic analyses of patients with severe spine segmentation defects have implicated several human orthologues of cyclic genes that are associated with the mouse segmentation clock, suggesting that this oscillator might be conserved in humans3. Here we show that human PSM cells derived in vitro-as well as those of the mouse4-recapitulate the oscillations of the segmentation clock. Human PSM cells oscillate with a period two times longer than that of mouse cells (5 h versus 2.5 h), but are similarly regulated by FGF, WNT, Notch and YAP signalling5. Single-cell RNA sequencing reveals that mouse and human PSM cells in vitro follow a developmental trajectory similar to that of mouse PSM in vivo. Furthermore, we demonstrate that FGF signalling controls the phase and period of oscillations, expanding the role of this pathway beyond its classical interpretation in 'clock and wavefront' models1. Our work identifying the human segmentation clock represents an important milestone in understanding human developmental biology." Coupling delay controls synchronized oscillation in the segmentation clock "Individual cellular activities fluctuate but are constantly coordinated at the population level via cell-cell coupling. A notable example is the somite segmentation clock, in which the expression of clock genes (such as Hes7) oscillates in synchrony between the cells that comprise the presomitic mesoderm (PSM)1,2. This synchronization depends on the Notch signalling pathway; inhibiting this pathway desynchronizes oscillations, leading to somite fusion3-7. However, how Notch signalling regulates the synchronicity of HES7 oscillations is unknown. Here we establish a live-imaging system using a new fluorescent reporter (Achilles), which we fuse with HES7 to monitor synchronous oscillations in HES7 expression in the mouse PSM at a single-cell resolution. Wild-type cells can rapidly correct for phase fluctuations in HES7 oscillations, whereas the absence of the Notch modulator gene lunatic fringe (Lfng) leads to a loss of synchrony between PSM cells. Furthermore, HES7 oscillations are severely dampened in individual cells of Lfng-null PSM. However, when Lfng-null PSM cells were completely dissociated, the amplitude and periodicity of HES7 oscillations were almost normal, which suggests that LFNG is involved mostly in cell-cell coupling. Mixed cultures of control and Lfng-null PSM cells, and an optogenetic Notch signalling reporter assay, revealed that LFNG delays the signal-sending process of intercellular Notch signalling transmission. These results-together with mathematical modelling-raised the possibility that Lfng-null PSM cells shorten the coupling delay, thereby approaching a condition known as the oscillation or amplitude death of coupled oscillators8. Indeed, a small compound that lengthens the coupling delay partially rescues the amplitude and synchrony of HES7 oscillations in Lfng-null PSM cells. Our study reveals a delay control mechanism of the oscillatory networks involved in somite segmentation, and indicates that intercellular coupling with the correct delay is essential for synchronized oscillation."

More recent papers

This table allows an automated computer search of the external PubMed database using the listed "Search term" text link. This search now requires a manual link as the original PubMed extension has been disabled. The displayed list of references do not reflect any editorial selection of material based on content or relevance. References also appear on this list based upon the date of the actual page viewing. References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability. More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Somitogenesis | Somite | Paraxial mesoderm | Presomitic Mesoderm | Sclerotome | Myotome | Dermatome |

Older papers

These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table. See also the Discussion Page for other references listed by year and References on this current page. Constraints on somite formation in developing embryos "Segment formation in vertebrate embryos is a stunning example of biological self-organization. Here, we present an idealized framework, in which we treat the presomitic mesoderm (PSM) as a one-dimensional line of oscillators. We use the framework to derive constraints that connect the size of somites, and the timing of their formation, to the growth of the PSM and the gradient of the somitogenesis clock period across the PSM. Our analysis recapitulates the observations made recently in ex vivo cultures of mouse PSM cells, and makes predictions for how perturbations, such as increased Wnt levels, would alter somite widths. Finally, our analysis makes testable predictions for the shape of the phase profile and somite widths at different stages of PSM growth. In particular, we show that the phase profile is robustly concave when the PSM length is steady and slightly convex in an important special case when it is decreasing exponentially. In both cases, the phase profile scales with the PSM length; in the latter case, it scales dynamically. This has important consequences for the velocity of the waves that traverse the PSM and trigger somite formation, as well as the effect of errors in phase measurement on somite widths.} Developmental dynamics of occipital and cervical somites "Development of somites leading to somite compartments, sclerotome, dermomyotome and myotome, has been intensely investigated. Most knowledge on somite development, including the commonly used somite maturation stages, is based on data from somites at thoracic and lumbar levels. Potential regional differences in somite maturation dynamics have been indicated by a number of studies, but have not yet been comprehensively examined. Here, we present an overview on the developmental dynamics of somites at occipital and cervical levels in the chicken embryo. We show that in these regions, the onset of sclerotomal and myotomal compartment formation is later than at thoracolumbar levels, and is initiated simultaneously in multiple somites, which is in contrast to the serial cranial- to- caudal progression of somite maturation in the trunk." Mesogenin 1 is a master regulator of paraxial presomitic mesoderm differentiation "Neuromesodermal (NM) stem cells generate neural and paraxial presomitic mesoderm (PSM) cells, which are the respective progenitors of the spinal cord and musculoskeleton of the trunk and tail. The Wnt-regulated basic helix-loop-helix (bHLH) transcription factor mesogenin 1 (Msgn1) has been implicated as a cooperative regulator working in concert with T-box genes to control PSM formation in zebrafish, although the mechanism is unknown. We show here that, in mice, Msgn1 alone controls PSM differentiation by directly activating the transcriptional programs that define PSM identity, epithelial-mesenchymal transition, motility and segmentation. Forced expression of Msgn1 in NM stem cells in vivo reduced the contribution of their progeny to the neural tube, and dramatically expanded the unsegmented mesenchymal PSM while blocking somitogenesis and notochord differentiation. Expression of Msgn1 was sufficient to partially rescue PSM differentiation in Wnt3a(-/-) embryos, demonstrating that Msgn1 functions downstream of Wnt3a as the master regulator of PSM differentiation." The precise timeline of transcriptional regulation reveals causation in mouse somitogenesis network "In vertebrate development, the segmental pattern of the body axis is established as somites, masses of mesoderm distributed along the two sides of the neural tube, are formed sequentially in the anterior-posterior axis. This mechanism depends on waves of gene expression associated with the Notch, Fgf and Wnt pathways." From dynamic expression patterns to boundary formation in the presomitic mesoderm "The segmentation of the vertebrate body is laid down during early embryogenesis. The formation of signaling gradients, the periodic expression of genes of the Notch-, Fgf- and Wnt-pathways and their interplay in the unsegmented presomitic mesoderm (PSM) precedes the rhythmic budding of nascent somites at its anterior end, which later develops into epithelialized structures, the somites. Although many in silico models describing partial aspects of somitogenesis already exist, simulations of a complete causal chain from gene expression in the growth zone via the interaction of multiple cells to segmentation are rare. Here, we present an enhanced gene regulatory network (GRN) for mice in a simulation program that models the growing PSM by many virtual cells and integrates WNT3A and FGF8 gradient formation, periodic gene expression and Delta/Notch signaling. Assuming Hes7 as core of the somitogenesis clock and LFNG as modulator, we postulate a negative feedback of HES7 on Dll1 leading to an oscillating Dll1 expression as seen in vivo. " FGF4 and FGF8 comprise the wavefront activity that controls somitogenesis "Somites form along the embryonic axis by sequential segmentation from the presomitic mesoderm (PSM) and differentiate into the segmented vertebral column as well as other unsegmented tissues. Somites are thought to form via the intersection of two activities known as the clock and the wavefront. ...Significantly, markers of nascent somite cell fate expand throughout the PSM, demonstrating the premature differentiation of this entire tissue, a highly unusual phenotype indicative of the loss of wavefront activity. When WNT signaling is restored in mutants, PSM progenitor markers are partially restored but premature differentiation of the PSM still occurs, demonstrating that FGF signaling operates independently of WNT signaling. This study provides genetic evidence that FGFs are the wavefront signal and identifies the specific FGF ligands that encode this activity. Furthermore, these data show that FGF action maintains WNT signaling, and that both signaling pathways are required in parallel to maintain PSM progenitor tissue."

Presomitic Mesoderm

Model for Sprouty4 and FGF in mesoderm segmentation

Within the mesodermal layer either side of the notochord (axial mesoderm) lie the paraxial mesoderm strips. Below the unsegmented cranial paraxial mesoderm region the region that will later segment is described as presomitic mesoderm (PSM). This PSM is being "patterned" by two two molecular activities described as the "clock" and the "wavefront" (reviewed) Many different molecular factors are involved in this patterning effect. Hes7, FGF, Sprouty4, Notch, Shh notochord influences somite formation, notochord removal increases the period of molecular clock oscillations.

‎‎Somitogenesis Page | Play

Human First Somites

Human embryo first somite pairs (week 4, Carnegie stage 9)

Somite Number

Week 4 to 5 (GA 6 to 7) covers the main period of human somitogenesis.

Human Embryo Somite Number

Week	Days	Carnegie Stage	Somite Number (pairs)
Week 3	19 - 21	9    image	1 - 3
Week 4	22 - 23	10   image	4 - 12
Week 4	23 - 26	11   image	13 - 20
Week 4	26 - 30	12   image	21 - 29
Week 5	28 - 32	13   image	30
Week 5	31 - 35	14   image	30+

Seel also Other species Somitogenesis

Mesoderm to Somite

Human embryo first somite pair (week 4, Carnegie stage 9)

Mesoderm means the "middle layer" and it is from this layer that nearly all the bodies connective tissues are derived. In early mesoderm development a number of transient structures will form and then be lost as tissue structure is patterned and organised. Humans are vertebrates, with a "backbone", and the first mesoderm structure we will see form after the notochord will be somites.

• During segmentation the outer cell layer forms an epithelial layer over a still mesenchymal organization of cells at the core.
• The early forming somite has a cavity at its core called a "somitocoel" that later fills with proliferating mesoderm cells.

Human embryo (week 4, Carnegie stage 11) Somites

• 

  paraxial mesoderm

• 

  early somite

Somite to Sclerotome and Dermomyotome

Sclerotome	Dermatome
sclerotome later becomes subdivided rostral and caudal halves separated laterally by von Ebner's fissure half somites contribute to a single vertebral level body other half intervertebral disc therefore final vertebral segmentation “shifts”	connective tissue underlying epidermis begins as a dorsal thickening spreads throughout the body
	Myotome
	Body - epaxial and hypaxial muscles Limbs - flexor and extensor muscles

Somite initially forms 2 main regional components

• ventromedial region - sclerotome forms vertebral body and intervertebral disc
• dorsolateral region - dermomyotome forms dermis and skeletal muscle

• 

  sclerotome and dermomyotome

• 

  dermatome and myotome

• 

  epaxial and hypaxial muscles

Sclerotome

Somite regions

• The left and right sclerotomes from the same segmental level engulf the notochord.
• Each segmental level is then resegmented in a rostrocaudal direction.

Dermomyotome

• The dermomyotome is divided into a dorsal and ventral half.
  • Dorsal - dermatome.
  • Ventral - myotome, this will also divide into a dorsal and ventral half that contribute the epaxial and hypaxial skeletal muscle groups respectively.

• hypaxial - muscles of the ventrolateral body wall, girdle, limb and tongue.
  • Muscle cells of the limb, tongue and lateral shoulder girdle muscles - derived from somite migrating myogenic precursor cells.
  • Muscle cells of the ventrolateral body wall muscles (intercostal and abdominal muscles) and the medial shoulder girdle muscles - derived from the myotome.

Part of the shoulder girdle muscles (trapezius and sternocleidomastoideus) - derived from the lateral plate mesoderm.

Molecular

During somitogenesis Dll1 protein appears to regulate clock genes, such as Hes7, expression oscillation in the presomitic mesoderm (PSM).

Hes7

Hairy/Enhancer Of Split, Drosophila, Homolog Of, 7 (HES7) 17p13.1 is a transcriptional repressor protein with teh structure containing a basic helix-loop-helix-Orange domain. It is a direct target of the Notch signaling pathway and also part of a negative feedback required to attenuate Notch signaling.

Links: OMIM - Hes7

Pax

Mesoderm Development and Pax

Links: Developmental Signals - Pax

Mesogenin 1

A master regulator of paraxial presomitic mesoderm differentiation.

Other Species

Animal Species - Average Somite Pair Number
Species	Somites Number
Human	44
Mouse	65
Chicken	55
Lizard (anole)	72-73
Xenopus	42
Zebrafish	32

Chicken

Chicken Somitogenesis
HH Stages	Age	Somite Number
7	23-26 hr	1 somite
7 to 8-	ca. 23-26 hr	1-3
8	26-29 hr	4
9	29-33 hr	7
9+ to 10-	ca. 33 hr	8-9
10	33-38 hr	10
11	40-45 hr	13
12	45-49 hr	16
13	48-52 hr	19
13+ to 14-	ca. 50-52 hr	20-21
14	50-53 hr	22
14+ to 15-	ca. 50-54 hr	23
15	50-55 hr	24-27
16	51-56 hr	26-28
17	52-64 hr	29-32
18	3 da	30-36
19	3.0-3.5 da	37- 40 extending into tail
20	3.0-3.5 da	40-43
21	3.5 da	43-44
22	3.5-4.0 da	Somites extend to tip of tail
Hamburger Hamilton Stages | Chicken Development

Chicken Somitogenesis
HH Stages	Age	Somite Number
7	23-26 hr	1 somite
7 to 8-	ca. 23-26 hr	1-3
8	26-29 hr	4
9	29-33 hr	7
9+ to 10-	ca. 33 hr	8-9
10	33-38 hr	10
11	40-45 hr	13
12	45-49 hr	16
13	48-52 hr	19
13+ to 14-	ca. 50-52 hr	20-21
14	50-53 hr	22
14+ to 15-	ca. 50-54 hr	23
15	50-55 hr	24-27
16	51-56 hr	26-28
17	52-64 hr	29-32
18	3 da	30-36
19	3.0-3.5 da	37- 40 extending into tail
20	3.0-3.5 da	40-43
21	3.5 da	43-44
22	3.5-4.0 da	Somites extend to tip of tail
Hamburger Hamilton Stages | Chicken Development

Mouse

Mouse Somitogenesis
Theiler Stages	Age E	(range dpc)	Somite Number	Rat Witschi Stage	Human Stage
12	8		1 - 7	14-15	9
13	8.5	(8 - 9.25)	8 - 12	15	10
14	9	(8.5 - 9.75)	13 - 20	16	11
15	9.5	(9 - 10.25)	21 - 29	17 - 19	12
16	10	(9.5 - 10.75)	30 - 34	20 - 21	13 - 15
17	10.5	(10 - 11.25)	35 - 39	24 - 25	13 - 15
18	11	(10.5 - 11.25)	40 - 44	25 - 26	13 - 15
19	11.5	(11 - 12.25)	45 - 47	26 - 27	16
20	12	(11.5 - 13)	48 - 51	28	17
21	13	(12.5-14)	52 - 55	29 - 30	18 - 19
22	14	(13.5-15)	56 - 60	31	20 - 23
23	15		60 +	32	Fetal period

Mouse Somitogenesis
Theiler Stages	Age E	(range dpc)	Somite Number	Rat Witschi Stage	Human Stage
12	8		1 - 7	14-15	9
13	8.5	(8 - 9.25)	8 - 12	15	10
14	9	(8.5 - 9.75)	13 - 20	16	11
15	9.5	(9 - 10.25)	21 - 29	17 - 19	12
16	10	(9.5 - 10.75)	30 - 34	20 - 21	13 - 15
17	10.5	(10 - 11.25)	35 - 39	24 - 25	13 - 15
18	11	(10.5 - 11.25)	40 - 44	25 - 26	13 - 15
19	11.5	(11 - 12.25)	45 - 47	26 - 27	16
20	12	(11.5 - 13)	48 - 51	28	17
21	13	(12.5-14)	52 - 55	29 - 30	18 - 19
22	14	(13.5-15)	56 - 60	31	20 - 23
23	15		60 +	32	Fetal period

Rat

Table III - Showing Means and Variation for Each Rat Age

				Maximum Variation
Age Days-Hrs.	Number of Litters	Number of Embryos Counted	Means	All Embryos	One Litter	Standard Deviation	Coefficient of Variation %
10-12	1	4	8.7	6-11	6-11	2.8	32
10-13	1	6 1	0. 2	8-13	8-13	1.9	19
10-16	2	12	12.4	6-26	6-26	5.8	47
10-17	6	48	12.9	4-26	7-26	3 .3	26
10-18	4	23	14.1	6-18	9-18	3.1	22
10-19	1	6	14 .3	12-17	12-17	1.2	8
10-22	3	16	13.1	6-19	6-14	3.9	30
10-23	3	17	15.2	8-18	8-18	2.4	16
11-00	2	0	14.6	10-17	10-17	1.9	13
11-02	2	15	20 . 9	17-22	17-22	1. 3	6
11-04	1	10	25. 3	23-26	23-26	1.2	5
11-06	1	2	18.0	18-18	18-18	.0	0
11-08	1	8	25 0	23-28	23-28	1.9	8
11-09	1	3	22 .0	20-25	20-25	2 . 2	10
11-10	2	18	26.2	21-31	21-31	2.9	11
11-11	3	26	25.6	14-29	14-27	3.2	12
11-12	1	3	26. 7	25-28	25-28	1.2	4
11-14	1	3	21.3	21-22	21-22	.6	2
11-15	1	8	23.1	17-28	17-28	4 . 0	17
11-16	1	7	26.7	24-28	24-28	1.3	5
11-17	1	7	26.1	25-28	25-28	1.1	4
11-18	3	25	25 .4	19-28	19-28	1.9	7
11-20	2	16	27.2	25-29	25-29	1.2	4
23 Ages	44	292				Av 2.2	Av 13%
Data Reference   Links: rat | somitogenesis

Table III Showing Means And Variation For Each Age
Table III - Showing Means and Variation for Each Rat Age Maximum Variation Age Days-Hrs. Number of Litters Number of Embryos Counted Means All Embryos One Litter Standard Deviation Coefficient of Variation % 10-12 1 4 8.7 6-11 6-11 2.8 32 10-13 1 6 1 0. 2 8-13 8-13 1.9 19 10-16 2 12 12.4 6-26 6-26 5.8 47 10-17 6 48 12.9 4-26 7-26 3 .3 26 10-18 4 23 14.1 6-18 9-18 3.1 22 10-19 1 6 14 .3 12-17 12-17 1.2 8 10-22 3 16 13.1 6-19 6-14 3.9 30 10-23 3 17 15.2 8-18 8-18 2.4 16 11-00 2 0 14.6 10-17 10-17 1.9 13 11-02 2 15 20 . 9 17-22 17-22 1. 3 6 11-04 1 10 25. 3 23-26 23-26 1.2 5 11-06 1 2 18.0 18-18 18-18 .0 0 11-08 1 8 25 0 23-28 23-28 1.9 8 11-09 1 3 22 .0 20-25 20-25 2 . 2 10 11-10 2 18 26.2 21-31 21-31 2.9 11 11-11 3 26 25.6 14-29 14-27 3.2 12 11-12 1 3 26. 7 25-28 25-28 1.2 4 11-14 1 3 21.3 21-22 21-22 .6 2 11-15 1 8 23.1 17-28 17-28 4 . 0 17 11-16 1 7 26.7 24-28 24-28 1.3 5 11-17 1 7 26.1 25-28 25-28 1.1 4 11-18 3 25 25 .4 19-28 19-28 1.9 7 11-20 2 16 27.2 25-29 25-29 1.2 4 23 Ages 44 292 Av 2.2 Av 13% Data Reference   Links: rat | somitogenesis
Reference: Landacre FL. and Amstutz MM. Data on the number of somites compared with age in the white rat. (1929) Ohio J. Science. 29(6): 253-259.

Additional Images

• 

  Model for Sprouty4 and FGF in mesoderm segmentation

• 

  Mouse (E8.5-9.5) somitogenesis gene expression

• 

  Mouse (E8.5) cleaved intracellular portion of Notch in unsegmented presomitic mesoderm (PSM)

• 

  Chicken body elongation model

References

Reviews

Takahashi Y & Sato Y. (2008). Somitogenesis as a model to study the formation of morphological boundaries and cell epithelialization. Dev. Growth Differ. , 50 Suppl 1, S149-55. PMID: 18482400 DOI.

Turnpenny PD. (2008). Defective somitogenesis and abnormal vertebral segmentation in man. Adv. Exp. Med. Biol. , 638, 164-89. PMID: 21038776

Kusumi K, Sewell W & O'Brien ML. (2008). Mouse mutations disrupting somitogenesis and vertebral patterning. Adv. Exp. Med. Biol. , 638, 140-63. PMID: 21038775

Mara A & Holley SA. (2007). Oscillators and the emergence of tissue organization during zebrafish somitogenesis. Trends Cell Biol. , 17, 593-9. PMID: 17988868 DOI.

Cinquin O. (2007). Understanding the somitogenesis clock: what's missing?. Mech. Dev. , 124, 501-17. PMID: 17643270 DOI.

Shifley ET & Cole SE. (2007). The vertebrate segmentation clock and its role in skeletal birth defects. Birth Defects Res. C Embryo Today , 81, 121-33. PMID: 17600784 DOI.

Aulehla A & Pourquié O. (2006). On periodicity and directionality of somitogenesis. Anat. Embryol. , 211 Suppl 1, 3-8. PMID: 17024300 DOI.

Brent AE. (2005). Somite formation: where left meets right. Curr. Biol. , 15, R468-70. PMID: 15964269 DOI.

Christ B, Huang R & Scaal M. (2004). Formation and differentiation of the avian sclerotome. Anat. Embryol. , 208, 333-50. PMID: 15309628 DOI.

Scaal M & Christ B. (2004). Formation and differentiation of the avian dermomyotome. Anat. Embryol. , 208, 411-24. PMID: 15338303 DOI.

Articles

Chu LF, Mamott D, Ni Z, Bacher R, Liu C, Swanson S, Kendziorski C, Stewart R & Thomson JA. (2019). An In Vitro Human Segmentation Clock Model Derived from Embryonic Stem Cells. Cell Rep , 28, 2247-2255.e5. PMID: 31461642 DOI.

O'Rahilly R & Müller F. (2003). Somites, spinal Ganglia, and centra. Enumeration and interrelationships in staged human embryos, and implications for neural tube defects. Cells Tissues Organs (Print) , 173, 75-92. PMID: 12649586 DOI.

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Cite this page: Hill, M.A. (2023, December 5) Embryology Somitogenesis. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Somitogenesis

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