Seed Germination and Seedling Growth

Theodore T. Kozlowski , Stephen G. Pallardy , in Growth Control in Woody Plants, 1997

Patterns of Seed Germination

Seed germination may be considered to be resumption of embryo growth resulting in seed coat rupture and emergence of the young plant. Growth of the embryo requires both cell division and elongation, cell division occurring first in some species and cell elongation in others. For example, cell division preceded cell elongation in embryo growth in Japanese black pine seeds (Goo, 1952). In cherry laurel, however, cell division and cell elongation began more or less simultaneously in embryonic organs (Pollock and Olney, 1959). Reserve foods in the seed sustain the growing embryo until the cotyledons and/or leaves expand to provide a photosynthetic system and roots develop to absorb water and minerals, thereby making the young plant physiologically self-sufficient. Seedlings of English walnut depended on reserve carbohydrates for respiratory substrates and growth for the first 21 days after the seeds were sown (Maillard et al., 1994). Photosynthesis was confirmed by day 22. At day 29 current photosynthetic products were used for 25 and 30% of the respiration of the root and shoot, respectively. Current photosynthate was incorporated into the shoot beginning on day 32 and into the taproot after 40 days. After 43 days the contribution of reserve carbohydrates to plant growth were negligible.

As the embryo resumes growth during seed germination, the radicle elongates and penetrates the soil. In some woody plants—including most gymnosperms, beech, dogwood, black locust, ash, and most species of maple—the cotyledons are pushed out of the ground by the elongating hypocotyl (epigeous germination). In other species—including oak, walnut, buckeye, and rubber—the cotyledons remain underground while the epicotyl grows upward and develops foliage leaves (hypogeous germination) (Figs. 2.3 and 2.4).

Figure 2.3. Stages in germination of seeds. (a) Germination of white oak acorns in which cotyledons remain below ground (hypogeous). (b) Germination of red maple in which cotyledons are pushed out of the ground (epigeous).

Figure 2.4. Epigeous germination of pine seed.

 Photo courtesy of St. Regis Paper Co.

Whereas all embryo cells divide during early seed germination, as seedlings develop the division of cells becomes localized in shoot and root apices. Important events following seed germination include sequential formation of leaves, nodes, and internodes from apical meristems. Shoots may originate from apical meristems in leaf axils, providing the young plant with a system of branches. The root apical meristem forms a taproot or primary root. Often branch roots or secondary roots originate at new apical meristems in the pericycle of the taproot.

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Glycosaminoglycans in Development, Health and Disease

Hiroko Habuchi , Koji Kimata , in Progress in Molecular Biology and Translational Science, 2010

E Aberrant Angiogenesis in the Placenta

It is thought that impaired placental function might be implicated in homozygous embryo growth retardation and/or perinatal lethality. HS of placenta from 15.5-day wild-type embryo had the higher content of nonsulfated disaccharide unit (HexA-GlcNAc) and the lower contents of 6- O-sulfated disaccharides units, compared with those of other tissues from neonatal mice (Fig. 6). In the placentas from the homozygous embryos, 6-O-sulfated disaccharide units almost disappeared with the exception of trisulfated disaccharide unit. Therefore, HS6ST-1 plays a particularly important role in HS biosynthesis in the placentas.

In comparison with the placental development of the homozygous and wild-type embryos by staining with hematoxylin/eosin, embryo-derived nucleated red cells that were abundant in the placentas of wild-type embryos were reduced in the placentas of homozygous embryos (Fig. 8). These observations suggest that angiogenesis should be impaired in the placentas of the HS6ST-1-deficient embryos. In fact, immunohistochemistry using anti-CD31 antibody, an antibody specific for vascular endothelial cells, supported such assumption. In the wild-type placentas, intense staining of numerous microvessels was observed in the labyrinthine zone, where the exchange of the nutrients and gases occurs (Fig. 9A ). In contrast, a weak staining of microvessels was observed in the labyrinthine zone of the HS6ST-1-deficient placentas. Analysis of these tissues by confocal microscopy showed that the number of microvessels in the homozygous placenta was reduced to about 60% of that in the wild-type placentas (Fig. 9B and C). Such an aberrant angiogenesis might jeopardize the nutritional supply and gas exchange in the HS6ST-1-deficient placentas.

Fig. 8. Comparison of placenta morphology in HS6ST-1+/+ (A, C) and HS6ST-1−/− (B, D) mice. The E15.5 placentas were stained with H & E. The lower panels show a higher magnification of the rectangle in the upper panels. The orange arrowheads indicate nucleated fetal red blood cells, and the green arrows indicate maternal red blood cells. In the labyrinthine zone of HS6ST-1−/− embryo placentas, there were a reduced number of fetal red blood cells. The yellow arrow indicates the labyrinthine zone. De, maternal deciduas; Ch, chorionic plate; La, labyrinthine zone; Sp, spongiotrophoblast layer. (Redrawn, with permission, from Ref. 41.) (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this chapter.)

Fig. 9. Reduced microvessels in the placenta of a homozygous embryo from a heterozygous mother. (A) Frozen sections from the E15.5 placentas were stained with an anti-CD31 antibody (green). (B) The left panel shows the photographs of a wild-type embryo, and the right panel shows the photographs of a homozygote embryo analyzed by confocal microscopy. (C) Bars indicate the mean number of microvessels in the labyrinthine zone per 5.3   ×   10−   8  mm2 counted from the photographs obtained from the confocal microscopic analysis. *p  <   0.03.

 (Redrawn, with permission, from Ref. 41.)

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Anatomy of Amphibians and Reptiles

Laurie J. Vitt , Janalee P. Caldwell , in Herpetology (Fourth Edition), 2014

Life in an Eggshell

Eggshells protect reptile embryos, but in so doing, impose special costs on embryo growth and physiology. An amphibian larva can grow to near adult size before metamorphosing, although most do not. A reptile in an eggshell cannot grow in size within the shell but must undergo complete development prior to hatching. By folding and curling, a reptile embryo can attain a surprising length, but it is still smaller than would be possible outside of a shell ( Fig. 2.5). Determinants of offspring size are complex and discussed elsewhere (see "Growth as a Life-History Trait" in Chapter 4). Most reptile hatchlings are, however, heavier than the mass of the original ovum. Metabolism of the yolk uses water absorbed through the shell, and the embryo grows beyond the original ovum.

FIGURE 2.5. Reptiles are tightly coiled inside of eggs prior to hatching. Embryos of Plestiodon fasciatus inside of eggs. Developmental stages 39 (upper) and 40 (lower) (James R. Stewart).

Just as temperature, water availability, and gas exchange affect the physiological processes of juveniles and adults, they also have the greatest impact on developing eggs. Eggs are not laid randomly in the environment. Females select sites that offer the greatest potential for egg and hatchling survival. Oviposition site selection has been honed by natural selection over generations of females. Nevertheless, abiotic and biotic environments are extremely variable, and eggs and their enclosed embryos must tolerate and respond to these varying conditions. A few examples illustrate the breadth of nesting environments and egg–embryo physiological responses.

Temperature tolerances of embryos lie typically within the tolerance range of the juveniles and adults of their species, but because the rate of development is temperature dependent and eggs lack the mobility to avoid extremes, exposure to extremes is likely to be fatal. At low temperatures, development slows down and hatching is delayed, resulting in emergence at suboptimal times or embryos that never complete development. At high temperatures, the embryo's metabolism increases exponentially so that yolk stores are depleted before development is completed, and of course, either extreme can be directly lethal by damaging cells and/or disrupting biochemical activity. Selection of protected oviposition sites potentially avoids extremes of temperature and provides a stable temperature environment. But temperatures do fluctuate within and among nests, and in some reptiles with temperature-dependent sex determination, skewed sex ratios among hatchlings can result from varying nest temperatures (see Chapter 5).

Moisture is no less critical for the proper development and survival of reptile embryos than for amphibians. However, amphibians typically require immersion in water, whereas immersion of most reptile eggs results in suffocation of embryos. Embryos do not drown, rather, the surrounding water creates a gaseous-exchange barrier at the shell–water interface, and the small amounts of gases that cross are inadequate to support cellular metabolism. The Australian sideneck turtle Chelodina rugosa avoids this dilemma, even though females lay their eggs in submerged nests. Once the eggs are laid, development stops. Developmental arrest typically occurs in the gastrulation phase, and embryogenesis begins only when the water disappears and the soil dries, permitting the eggs and/or the embryos to respire. The relative availability of water affects the rate of development and absolute size of the hatchlings. For example, eggs of the turtle Chrysemys picta hatch sooner and produce larger hatchlings in high-moisture nests than those in nests with lower moisture. Developmental abnormalities can also result if hatchlings experience dehydration as embryos.

Adequate gas exchange is an unlikely problem for species that lay or attach their eggs openly in cavities or crevices (e.g., many geckos), but for the majority of reptiles that bury their eggs, adequate gas exchange can be critical. Changes in soil permeability affect the diffusion of air, drier soils having the highest diffusion rates and wet soils the lowest. Similarly, soil friability and associated aspects of particle size and adhesiveness influence movement of gas through soil. Nest site selection is poorly understood for most reptiles, although consequences of nest site selection have received considerable attention. How can a female select a site that will avoid nest predation and maintain appropriate temperatures and humidity during an extended time period, considering the vagaries of temporal variation in local weather?

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Fetal Alcohol Syndrome and Fetal Alcohol Effects: A Clinical Perspective of Later Developmental Consequences

Ann Pytkowicz Streissguth , in Maternal Substance Abuse and the Developing Nervous System, 1992

INTRODUCTION

Alcohol is now well recognized as a teratogenic drug: prenatal exposure can cause death to the embryo and fetus, growth deficiency, malformations, and central nervous system aberrations that can last a lifetime. Whereas definitive documentation of the etiology and mechanisms comes from the experimental animal literature (see Goodlett and West, Chapter 4), the clinical literature is important in understanding the significant impact of this most widely used teratogen on our children. The epidemiologic literature is relevant for establishing public policy and guiding programs of prevention for this most preventable cause of mental retardation and developmental disability, and understanding the clinical phenomena of fetal alcohol syndrome (FAS) and fetal alcohol effects (FAE) is essential for developing appropriate treatment and intervention programs for affected children so that they can lead as productive and fulfilling lives as possible. There has been a shocking paucity of such research in the United States in the past 18 years since FAS was identified.

Fetal alcohol syndrome is generally recognized as the leading known cause of mental retardation (Abel and Sokol, 1987), surpassing Down's syndrome and spina bifida. (Most mental retardation cannot be attributed to a specific etiology.) Precise figures on FAS are difficult to obtain, however, and it seems likely that most attempts at estimating prevalence [including those most recently proposed by Abel and Sokol (1991)] are underestimates owing to difficulties with ascertainment and identification, confusion over diagnostic criteria, and problems in making interpretations based on literature surveys, including studies of variable validity. FAS is a clinical diagnosis (see below). The term FAS does not include all individuals affected by alcohol in utero, but rather it represents one specific and identifiable end of the continuum of disabilities caused by maternal alcohol use during pregnancy.

The clinical features of FAS were independently identified in France (Lemoine et al., 1968) and the United States (Jones et al., 1973; Jones and Smith, 1973). Most of the patients described have been infants or young children, but increasingly maladaptive behaviors among adolescents with FAS (Streissguth et al., 1991) make this an important topic for further study. A systematic examination of all school-age children with only mild mental retardation (IQ 55 to 70), born in Sweden during a 2-year period, indicated that 8% were afflicted with alcohol-related disabilities (Hagberg et al., 1981a,b). A recent report involving ophthalmology examinations of this same cohort raised the proportion with suspected FAS to 10% [a larger proportion than was identified by all known genetic disorders (Hagberg et al., 1981a,b; Stromland, 1990)]. Enough is currently known to indicate that FAS is a major health problem. The fact that precise figures are not available should not dissuade us from recognizing the urgency of the need for research on the characteristics and special needs of this underserved population of disabled persons.

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Female Infertility

Robert L. Barbieri , in Yen and Jaffe's Reproductive Endocrinology (Eighth Edition), 2019

Luteal Phase Deficiency

Luteal phase deficiency has been defined as a condition in which the ovarian secretion of progesterone is not sufficient to maintain a functional secretory endometrium that supports embryo implantation and growth. The gold standard test for identifying luteal phase deficiency is histologic dating of tissue from an endometrial biopsy that demonstrates a developmental lag of at least 2 days. However, most recent research indicates that delayed maturation of the endometrium is observed at a similar rate in both fertile and infertile women. 127 Most authorities believe that luteal phase deficiency is not a major independent cause of infertility. 128

From an endocrine perspective, follicular or luteal function that is far outside the normative range is likely associated with reduced fertility. In the most extreme example, it is known that resection of the corpus luteum and the associated reduction in progesterone secretion reduces fertility and causes abortion in women prior to about 49 days of pregnancy. 129 In addition, numerous clinical trials have observed that luteal phase progesterone support improves pregnancy rates following IVF cycles involving controlled ovarian hyperstimulation and ovarian follicle puncture to harvest oocytes. 130 It is probable that an occasional case of infertility may be caused by poor follicle development and inadequate corpus luteal secretion of progesterone or a relative resistance to progesterone effect in the endometrium. However, it is unlikely that luteal phase deficiency is a common cause of infertility.

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Genomic imprinting

Sharvari Deshpande , ... N.H. Balasinor , in Epigenetics and Reproductive Health, 2021

Genomic imprinting in embryogenesis

Nuclear transplantation experiments in mice demonstrated the distinct roles of the two parental genomes in embryogenesis. In addition, the first identified imprinted genes were shown to be essential for normal embryo growth.

The most well-studied imprinted gene cluster that regulates embryo growth is the IGF2-H19 cluster, which has two imprinted genes, namely, IGF2 and H19. IGF2 is expressed from the paternal allele and is a positive regulator of embryo growth. Biallelic expression of Igf2 results in embryonic overgrowth, whereas its reduction leads to growth restriction [6,27,41]. H19, a non-coding RNA, is expressed from the maternal allele and is a negative regulator of embryo growth [46]. IGF2 binds to two receptors, IGF1r and IGF2r. Binding to IGF1r, IGF2 promotes embryo growth, however, IGF2 binding to IGF2r, a maternally expressed imprinted gene, targets it for lysosomal degradation [43].

Besides Igf2, Igf2r and H19, a number of imprinted genes are reported to have an effect on embryonic growth, namely Grb10, Peg1 (Mest), Gtl2 (Meg3), Cdkn1c, Plagl1 (Zac1) and Dlk1. Grb10 is maternally expressed in most murine tissues and acts as a growth restrictor. Maternal Grb10-knockout embryos exhibit overgrowth. Deletion of the Grb10 ICR results in its biallelic expression and significant undergrowth [16,113]. It has been shown that embryonic growth is regulated by Imprinted Gene Network (IGN) involving a number of imprinted genes, including Igf2, Peg1 (Mest), Gtl2 (Meg3), Cdkn1c, Plagl1 and Dlk1. Studies by Varrault et al. demonstrated that about 15 imprinted genes are coordinately regulated in multiple tissues forming an IGN. Zac1 (Plagl1) a paternally expressed imprinted gene regulates the IGN [125]. Deletion of Zac1 gene in mice results in intrauterine growth restriction and neonatal lethality. ZAC1 alters the expression of several imprinted genes, including Cdkn1c and Dlk1, and directly regulates the H19/Igf2 locus [125]. In addition to Zac1, H19 is a possible regulator of the IGN [46] and BMI1, a member of the Polycomb Repressive Complex 1 (PRC1) has also been shown to be implicated in the synchronized expression of multiple imprinted genes within this network [140].

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The Platelet as a Physiological Object in the Circulation

A.H. Marshall , ... H. Ni , in Pathobiology of Human Disease, 2014

Angiogenesis

In addition to hemostasis and the immune system, platelets contribute to angiogenesis: the process of new blood vessel growth, which has implications for wound healing, tumorigenesis, and embryo and fetal growth. Platelet granules contain proangiogenic factors including vascular endothelial growth factor (VEGF), angiopoietin 1, platelet-derived growth factor, insulin-like growth factor, hepatocyte growth factor, fibroblast growth factor, epidermal growth factor, CXCL12 (SDF-1α), and matrix metalloproteinases (MMP1, 2, and 9). Platelet-derived proangiogenic factors increase vessel wall permeability and promote endothelial cell, progenitor cell, and fibroblast recruitment, growth, and proliferation. They also contain and release antiangiogenic factors endostatin, angiostatin, TSP-1, platelet factor 4, and plasminogen activator inhibitor 1. TSP-1, for example, can potently inhibit endothelial cell proliferation and even initiate endothelial cell apoptosis.

Platelets contribute to wound healing. In vitro, platelets stimulate endothelial cell tube formation on Matrigel. In murine models, Dr. Wagner's group provided evidence that platelets and platelet adhesion support angiogenesis while preventing hemorrhage. Interestingly, Dr. Joseph Italiano's and Dr. Nailin Li's groups demonstrated that pro- and antiangiogenic factors are stored in separate α granules in platelets and megakaryocytes and are selectively released depending on the pathway of platelet activation. Platelet activation via PAR-4 causes endostatin (not VEGF) granule release. By contrast, platelet activation via PAR-1 leads to VEGF (not endostatin) granule release. Other researchers have demonstrated that ADP, PAR-1, and GPVI support release of proangiogenic factors, while PAR-4 and TXA2 lead to release of antiangiogenic factors.

Despite the reported antitumor actions of platelets, evidence suggests that cancer cells are able to manipulate platelets into supporting tumorigenesis. Although platelet-derived TSP-1 is a critical negative regulator during the early stages of tumor angiogenesis, eventually, cancer cells seem to manipulate platelets to release their proangiogenic proteins. Dr. Italiano's group reported that platelets release VEGF and other proangiogenic factors after exposure to breast cancer cells in vitro. Moreover, Dr. Wagner's group demonstrated that platelets and platelet granule contents protect tumor vasculature and intratumor hemorrhage in vivo. These findings explain observations by Dr. Trousseau and others that thromboembolism (when a thrombus separates from the initial site of adhesion and circulates to another site) correlates with tumor malignancy and that elevated platelet count correlates with mortality in several types of cancer. Consistent with these observations, thrombocytopenia in mice reduced metastases, increased vascular leakage of tumor vessels, and increased the efficacy of chemotherapy. Overall, platelets seem to support tumor growth by promoting angiogenesis.

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Tick heme-binding aspartic proteinase

Marcos Henrique Ferreira Sorgine , ... Luiz Juliano , in Handbook of Proteolytic Enzymes (Second Edition), Volume 1, 2004

Biological Aspects

In the tick egg, THAP is associated with the yolk granules (M.H.F. Sorgine, E.A. Machado, L. Juliano & P.L. Oliveira (unpublished)). For this reason, it has been proposed that the physiological role of this protein is to degrade vitellin (VT), the major storage protein from eggs of arthropods, releasing amino acids that will support embryo growth. Since tick VT is a heme protein, THAP could use its heme-binding site as a docking site to bind heme molecules exposed at the surface of VT, thereby increasing its affinity towards this substrate and leading to more efficient degradation. On the other hand, if the degradation of VT releases high levels of free heme (a potentially toxic molecule, capable of generating free radicals), this heme may bind to the THAP heme-binding site, providing a negative feedback regulation, slowing the pace of VT degradation until the excess heme is removed from the yolk granule.

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Tick Heme-Binding Aspartic Proteinase

Marcos Henrique Ferreira Sorgine , ... Luiz Juliano , in Handbook of Proteolytic Enzymes (Third Edition), 2013

Biological Aspects

Pohl et al. [3] have shown that in the tick egg, THAP associates with the yolk granules, a cellular localization identical to the other aspartic proteinase found in tick eggs, BYC [4] . For this reason, it has been proposed that the physiological role of the protein is to degrade vitellin (VT), the major storage protein in eggs of arthropods, releasing amino-acids that will support embryo growth. Interestingly, these authors have shown that THAP presents differential activity when assayed against VTs purified from different days after egg-laying, with maximum activity against the protein from 7-day eggs. It has been proposed, that since tick VT is a hemeprotein, THAP could use its heme-binding site as a docking site, to bind heme molecules exposed at the surface of VT, thereby increasing its affinity towards this substrate and leading to more efficient degradation. On the other hand, if the degradation of VT releases high levels of free heme (a potentially toxic molecule, capable of generating free radicals), this heme can bind to the THAP heme-binding site providing a negative feedback regulation, slowing the pace of VT degradation until the excess of heme is removed from the yolk granules.

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Yolk Cathepsin (Boophilus sp.)

Marcos Henrique Ferreira Sorgine , Maria Clara Leal Nascimento-Silva , in Handbook of Proteolytic Enzymes (Third Edition), 2013

Biological Aspects

In the tick egg, BYC was immunolocalized in yolk granules and small vesicles associated to it, especially in the most cortical granules, which are acidified upon the formation of the embryo syncytial blastoderm, four days after oviposition. For this reason, it has been proposed that the physiological role is to degrade VT, the major storage protein from eggs of arthropods, releasing amino-acids that will support embryo growth. It is proposed that during the course of embryo development, vesicles containing BYC fuse with the peripheral yolk granules which are acidified through the activation of H+-pumping ATPases. This activation would lead to BYC autocatalytic activation and to VT degradation. This fact is reinforced by the high specificity of this protein towards degradation of vitellin in comparison to several other substrates [10].

Recently, it was shown by Estrela et al. [11] that BYC can also be purified from Rhipicephalus (Boophilus) microplus larvae. In this case, it was proposed that BYC, along with a cysteine proteinase named Rhipicephalus microplus larval cysteine endopeptidase (RmLCE) would be involved in degradation of hemoglobin and VT by the larvae. It is shown that the degradation of Hb is synergically increased upon incubation with these two enzymes together, which led the authors to propose the existence of an Hb-degrading enzymatic cascade involving these enzymes in the tick larvae [11].

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