Plant Cytogenetics: Inheritance of Lethal genes.
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Prepared for B. Sc. III Botany students, based on the syllabus prescribed by Dr. Babasaheb Ambedkar Marathwada University, Aurangabad.
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severe combined immunodeficiency
Severe combined immunodeficiency (SCID) is a genetic disorder characterized by the absence of functional T lymphocytes and B lymphocytes, resulting in impaired adaptive immune system. There are several known types of SCID caused by mutations in different genes. The most common treatment is bone marrow transplantation, with success seen in transplants done in early infancy. Gene therapy is also being explored as a potential treatment through inserting missing genes into hematopoietic stem cells, though past trials increased leukemia risk and more research is still needed.
Lethal genes
Lethal genes are genes that lead to the death of an organism. There are several types of lethal genes including early onset lethal genes that cause death during embryogenesis, late onset lethal genes that have delayed effects causing death over time, conditional lethal genes that only kill under certain environmental conditions, and semi-lethal genes that kill some but not all individuals. Some of the first observations of lethal genes included work in 1907 by E. Baur on snapdragon plants where homozygous aurea plants lacked chlorophyll and died, and work in 1905 by L. Cuenot on mouse coat color inheritance where yellow mice could not be obtained in homozygous condition.
severe combined immunodeficiency syndrome
Severe combined immunodeficiency syndrome (SCID) is a rare genetic disorder characterized by the absence of both T cells and B cells. This leaves the body unable to fight infections and affected infants often develop severe, life-threatening infections within the first year of life if untreated. There are 13 known genetic causes of SCID. The main treatment is a bone marrow transplant from a matched donor, which can cure the condition if performed early in life. Gene therapy is also being explored as a potential treatment.
Summary modified
immunlogy case report done by Areen Mitt'b talk about Severe combined immunodeficiency omenn syndrome
uploded by Abbas W. Abbas
Severe combined immunodeficiency [compatibility mode]
Severe combined immunodeficiency is a primary immune deficiency that causes problems with T cells and B cells, leading to frequent infections, skin infections, failure to grow, and fungal infections. It can be fatal if not treated early in an infant's life. The disorder is caused by genetic defects linked to the X chromosome or chromosomes 19 and 20, including defects in the ADA and IL2RG genes. Treatments include bone marrow transplants from identical donors, living in a sterile bubble, and gene therapy, though the latter is not always successful.
Severe combined immunodeficiency
Severe combined immunodeficiency (SCID) is a group of genetic disorders where the immune system is missing or not functioning properly, resulting in little to no immune response. The two most common types are X-linked SCID, caused by a mutation on the X chromosome preventing the development of T cells, and adenosine deaminase deficiency SCID, where a lack of the enzyme adenosine deaminase prevents maturation of lymphocytes. Without treatment like bone marrow transplant or gene therapy, patients with SCID develop serious infections very early in life.
Combined Immunodeficiency
This document summarizes combined immunodeficiency (CID), a disorder characterized by defects in the production or maturation of T cells and/or B cells, leaving the body without necessary immunity. There are two main types of CID - mutagenic defects due to genetic mutations and enzyme deficiencies from lack of enzymes. Mutagenic CIDs can be autosomal recessive or X-linked. Treatments discussed include bone marrow transplantation, gene therapy, passive antibody administration, and enzyme replacement.
severe-combined-immunodeficiency
Severe combined immunodeficiency (SCID), also known as "bubble boy disease", is a genetic disorder where the immune system is impaired or absent. It affects both B cells and T cells. SCID can be diagnosed through newborn screening and symptoms include life-threatening infections in the first months of life. Treatment options include preventing infections, enzyme therapy for some types of SCID, gene therapy, and bone marrow transplantation which has been successful using matched or half-matched donors. The original "bubble boy" David Vetter died after transplantation due to an unscreened virus in his donor marrow.
Recommended
severe combined immunodeficiency
Severe combined immunodeficiency (SCID) is a genetic disorder characterized by the absence of functional T lymphocytes and B lymphocytes, resulting in impaired adaptive immune system. There are several known types of SCID caused by mutations in different genes. The most common treatment is bone marrow transplantation, with success seen in transplants done in early infancy. Gene therapy is also being explored as a potential treatment through inserting missing genes into hematopoietic stem cells, though past trials increased leukemia risk and more research is still needed.
Lethal genes
Lethal genes are genes that lead to the death of an organism. There are several types of lethal genes including early onset lethal genes that cause death during embryogenesis, late onset lethal genes that have delayed effects causing death over time, conditional lethal genes that only kill under certain environmental conditions, and semi-lethal genes that kill some but not all individuals. Some of the first observations of lethal genes included work in 1907 by E. Baur on snapdragon plants where homozygous aurea plants lacked chlorophyll and died, and work in 1905 by L. Cuenot on mouse coat color inheritance where yellow mice could not be obtained in homozygous condition.
severe combined immunodeficiency syndrome
Severe combined immunodeficiency syndrome (SCID) is a rare genetic disorder characterized by the absence of both T cells and B cells. This leaves the body unable to fight infections and affected infants often develop severe, life-threatening infections within the first year of life if untreated. There are 13 known genetic causes of SCID. The main treatment is a bone marrow transplant from a matched donor, which can cure the condition if performed early in life. Gene therapy is also being explored as a potential treatment.
Summary modified
immunlogy case report done by Areen Mitt'b talk about Severe combined immunodeficiency omenn syndrome
uploded by Abbas W. Abbas
Severe combined immunodeficiency [compatibility mode]
Severe combined immunodeficiency is a primary immune deficiency that causes problems with T cells and B cells, leading to frequent infections, skin infections, failure to grow, and fungal infections. It can be fatal if not treated early in an infant's life. The disorder is caused by genetic defects linked to the X chromosome or chromosomes 19 and 20, including defects in the ADA and IL2RG genes. Treatments include bone marrow transplants from identical donors, living in a sterile bubble, and gene therapy, though the latter is not always successful.
Severe combined immunodeficiency
Severe combined immunodeficiency (SCID) is a group of genetic disorders where the immune system is missing or not functioning properly, resulting in little to no immune response. The two most common types are X-linked SCID, caused by a mutation on the X chromosome preventing the development of T cells, and adenosine deaminase deficiency SCID, where a lack of the enzyme adenosine deaminase prevents maturation of lymphocytes. Without treatment like bone marrow transplant or gene therapy, patients with SCID develop serious infections very early in life.
Combined Immunodeficiency
This document summarizes combined immunodeficiency (CID), a disorder characterized by defects in the production or maturation of T cells and/or B cells, leaving the body without necessary immunity. There are two main types of CID - mutagenic defects due to genetic mutations and enzyme deficiencies from lack of enzymes. Mutagenic CIDs can be autosomal recessive or X-linked. Treatments discussed include bone marrow transplantation, gene therapy, passive antibody administration, and enzyme replacement.
severe-combined-immunodeficiency
Severe combined immunodeficiency (SCID), also known as "bubble boy disease", is a genetic disorder where the immune system is impaired or absent. It affects both B cells and T cells. SCID can be diagnosed through newborn screening and symptoms include life-threatening infections in the first months of life. Treatment options include preventing infections, enzyme therapy for some types of SCID, gene therapy, and bone marrow transplantation which has been successful using matched or half-matched donors. The original "bubble boy" David Vetter died after transplantation due to an unscreened virus in his donor marrow.
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Severe combined immunodeficiency (SCID), also known as bubble boy disease, is a genetic disorder where both the B cell and T cell arms of the immune system are impaired. There are several types of SCID resulting from defects in different genes. Symptoms include life-threatening infections from an early age. Treatment involves preventing infections, enzyme therapy, gene therapy, or bone marrow transplant from a matched or half-matched donor to rebuild the immune system. Transplants have been successful but carry risks, as seen in the original "bubble boy" who died from a virus in his transplanted marrow.
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2. It explains the molecular basis of mutations including that DNA contains genetic instructions encoded by sequences of bases and that mutations occur when the DNA sequence changes.
3. The causes of mutations are discussed as DNA replication errors, external influences like chemicals or radiation, and during processes like genetic recombination.
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Lethal Gene.pptx
Lethal genes are genes that cause death or reduced viability in individuals carrying them. Some lethal genes cause death early in development like at the zygote or embryonic stage, while others act later in development. There are three main types of lethal genes: recessive lethals, which only cause death when homozygous; dominant lethals, which reduce viability even in heterozygotes; and conditional lethals, which require a specific condition like temperature to express their lethal effects. One of the first lethal genes discovered was the Y gene in mice, which causes death when homozygous (YY) but not when heterozygous (Yy).
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The novel coronavirus SAR CoV 2 has resulted in huge wave of worldwide fear by its contagious nature, virulence and high mortality. Persistence condition of the disease with T cells and Natural killer cells exhaustion leads to Lymphopenia or Lymphocytopenia. Lymphocytopenia is a condition of low lymphocyte count in the blood. Lymphocytopenia is an important adverse effect of COVID 19 as well as negative prognostic marker in many malignancies. It leads to hyper activation of immune system that can cause immunosuppression and promote cytokine storm that eventually leads to multi organ failure and death. Restoration of lymphocytes and its function would be helpful to boost the immune response against COVID 19 disease. This review analyses the possible causes that may lead to the lymphocyte reduction in COVID 19 patients, and highlighting the possible therapeutic strategies that will help to control and prevent lymphocytopenia in COVID 19 patients. Shatabdi Dey | P. K Sahoo "Lymphocytopenia and COVID19: A Literature Review" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-5 | Issue-2 , February 2021, URL: https://www.ijtsrd.com/papers/ijtsrd38373.pdf Paper Url: https://www.ijtsrd.com/biological-science/immunobiology/38373/lymphocytopenia-and-covid19-a-literature-review/shatabdi-dey
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Severe combined immunodeficiency
Severe combined immunodeficiency (SCID), also known as bubble boy disease, is a genetic disorder where both the B cell and T cell arms of the immune system are impaired. There are several types of SCID resulting from defects in different genes. Symptoms include life-threatening infections from an early age. Treatment involves preventing infections, enzyme therapy, gene therapy, or bone marrow transplant from a matched or half-matched donor to rebuild the immune system. Transplants have been successful but carry risks, as seen in the original "bubble boy" who died from a virus in his transplanted marrow.
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Publications and conferences
This document provides a list of publications and conference presentations by Tian L. The publications section lists 10 peer-reviewed journal articles published between 2014-2009 covering topics related to T cell receptor signaling, regulatory T cells, autoimmunity, and CD8+ T cell differentiation. The conferences section lists 3 conferences between 2012-2010 where Tian L presented oral presentations on immune tolerance and regulatory T cells.
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We hear much about mutations that cause terrible diseases, but this presentation identifies several genetic mutations that result in improved health.
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C.A. Guerber et al.
This study examined the biochemical responses and plant survival of summer dormant and summer active tall fescue populations under drought conditions. Two summer dormant tall fescue populations and one summer active cultivar were grown with and without endophyte under non-irrigated conditions at humid and semi-arid sites. The summer dormant populations had lower expression of dehydrins, superoxide dismutase, and phenolic compounds compared to the summer active cultivar, indicating reduced metabolic activity. However, the summer dormant populations achieved 96-99% survival while the summer active cultivar had lower survival rates. The results suggest summer dormancy allows for reduced biochemical activity and improved drought survival in tall fescue.
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1. The presentation discusses various types of mutations including substitutions, insertions, deletions, and frameshifts.
2. It explains the molecular basis of mutations including that DNA contains genetic instructions encoded by sequences of bases and that mutations occur when the DNA sequence changes.
3. The causes of mutations are discussed as DNA replication errors, external influences like chemicals or radiation, and during processes like genetic recombination.
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Similar to Plant Cytogenetics: Inheritance of Lethal genes.
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This document discusses different types of genes including: complementary genes, duplicate genes, polymeric genes, modifying genes, and lethal genes. It provides examples of each gene type and how they interact to influence inheritance and traits. Complementary genes require two genes to work together to produce a trait. Duplicate genes have the same effect on a trait. Polymeric genes have an additive effect. Modifying genes influence other genes. Lethal genes cause death and can be dominant, recessive, sex-linked, or conditional.
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This document discusses how environmental factors can influence gene expression. It provides examples of how temperature, light, chemicals, and nutrition can all impact the expression of genes in rabbits, maize plants, fish embryos, and humans. The document also covers different types of lethal alleles, including recessive, dominant, conditional, sex-linked, and conditional lethal alleles. Recessive lethal alleles do not cause death unless an organism carries two copies, while dominant lethal alleles are expressed in both homozygotes and heterozygotes. Conditional lethal alleles only cause death when certain environmental changes are introduced. Sex-linked lethal alleles are carried on the X chromosome.
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Geneticsand heredity
Gregor Mendel was an Austrian monk who is considered the father of genetics. In the mid-1800s, he conducted experiments breeding pea plants and discovered the basic principles of heredity. He found that traits are passed from parents to offspring through discrete factors that we now call genes. Mendel's work laid the foundation for modern genetics and showed that inheritance follows specific biological rules.
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This document summarizes key concepts in genetics and heredity. It defines variations as differences between individuals of a species, which can provide advantages and allow selection by the environment. Heredity determines which traits are reliably passed from parents to offspring. The document discusses Gregor Mendel's experiments with pea plants that established the laws of inheritance, including his studies of monohybrid and dihybrid crosses. It also notes that sex determination varies between species, with human sex being largely genetically determined by inheritance of X or Y chromosomes from the father.
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These notes are intended for studies and you should also read other works by different persons to have and gain more knowledge
GENETICS-AND-HEREDITY: an overview to genetics
Gregor Mendel conducted breeding experiments with pea plants in the 1860s and discovered the basic laws of inheritance. Through his work breeding and tracking thousands of pea plants over many generations, Mendel was able to deduce that traits are passed from parents to offspring through discrete units, now known as genes, and that these genes assort and segregate based on mathematical probabilities. Mendel's discoveries laid the foundation for genetics as a science, though his work was not widely recognized until after his death.
GENETIC DISORDER IN LIVESTOCK ANIMAL
Genetic disorders can occur in livestock animals due to mutations in genes or chromosomal abnormalities. In cattle, common genetic disorders include dwarfism, osteopetrosis (marble bone disease), tibia hemimelia, and pulmonary hypoplasia with anasarca. Sheep disorders include spider lamb syndrome and rectal prolapse. Chicken disorders include bent toes and split wings. Goats can experience epidermolysis bullosa or the fainting goat condition. Prevention of genetic disorders in livestock is important for economic reasons and involves selective breeding practices like culling affected animals and avoiding inbreeding to reduce homozygosity.
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This document discusses various ways that alleles can alter phenotypes and modify Mendelian ratios. It describes different types of mutations that can cause loss or gain of function. It also explains genetic symbols used to represent alleles and different inheritance patterns such as incomplete dominance, codominance, lethal alleles, and epistasis. Multiple examples are provided to illustrate these concepts, such as coat color in mice, fruit color in squash, and flower color in peas. The key point is that while principles of segregation and independent assortment still hold, gene interactions can produce novel phenotypes and modified dihybrid ratios expressed in sixteenths.
Genetic basis of inheritance
Genetics is the study of genes and heredity. Gregor Mendel conducted experiments with pea plants in the mid-1800s and is considered the father of genetics. Through his experiments, he discovered the basic principles of inheritance, including dominant and recessive traits, alleles, and the particulate nature of inheritance. Mendel's work laid the foundation for modern genetics and our understanding of how traits are passed from parents to offspring.
Extension to Mendel's Law - 2015/02/20
This document discusses several concepts related to genetics:
1. It describes incomplete dominance and codominance, using the example of flower color in petunias.
2. It explains lethal alleles and how they can cause death in homozygous or heterozygous individuals. Examples given include coat color in mice and genes in cattle and humans.
3. Multiple alleles are discussed, which have varying levels of dominance and control traits like eye color in fruit flies and coat color in rabbits.
Beyond Mendel's laws of Inheritance.pdfa
This document discusses several concepts that extend beyond Mendel's laws of inheritance:
- Incomplete dominance occurs when neither allele of a gene is fully dominant, resulting in an intermediate phenotype in heterozygotes. Examples given include flower color in plants and cholesterol levels in humans.
- Multiple alleles exist when a gene has more than two alleles in a population. The ABO blood group in humans, which has A, B, and O alleles, is provided as an example.
- Sex-linked traits involve genes located on the X or Y chromosome, rather than autosomal chromosomes. Examples of X-linked traits that mainly affect males like hemophilia and Duchenne muscular dystrophy are described.
Heredity and evolution of biology topic b
This document provides information about heredity and evolution. It defines key genetics terms like heredity, variation, genetics, and discusses Gregor Mendel's experiments with pea plants that established the laws of inheritance. Mendel's work demonstrated that traits are passed from parents to offspring through discrete units called genes. The document also covers sex determination in humans and other animals.
Genetic
This document discusses human genetics and genetic disorders. It begins by noting statistics on genetic abnormalities in newborns and diseases with a genetic component. It then defines genetics, genomics, proteomics, and single nucleotide polymorphisms. The rest of the document discusses molecular bases of human disease including functional and positional cloning. It classifies human diseases and discusses mutations, Mendelian disorders, X-linked disorders, and autosomal dominant and recessive patterns of inheritance. Key points covered include definitions of genetic terms, Mendel's laws of inheritance, mechanisms of various disorders, and inheritance patterns.
Class _X_Science_Heredity and evolution_PPT pdf.pptx
Gregor Mendel performed experiments on garden peas to formulate the laws of genetics. He conducted monohybrid and dihybrid crosses to study the inheritance of single and double pairs of traits. His experiments showed that traits are transmitted from parents to offspring through discrete units of heredity called factors, now known as genes. The phenotype is the observable physical trait, while the genotype is the genetic makeup underlying the phenotype.
Experimental research
1. Frederick Griffith conducted an experiment in 1928 that showed a "transforming principle" in bacteria, demonstrating that genetic information could be transferred between bacterial strains.
2. He found that mice injected with a mixture of dead, heat-killed bacteria and live bacteria died, and the bacteria in their blood showed a transformation from the normally harmless strain to the deadly strain.
3. This established that some kind of genetic information was being transferred, pioneering the discovery of DNA as the mechanism of inheritance over 30 years later.
3.4 inheritance
Mendel discovered inheritance principles through pea plant experiments. Gametes contain one allele per gene. During meiosis, alleles separate and recombine in offspring. Dominant alleles mask recessives. Many human genetic diseases are recessive traits on autosomes, though some are dominant, codominant, or sex-linked. Punnett squares can predict offspring genotypes from parental alleles. Test crosses determine if an individual is homozygous or heterozygous dominant. Multiple alleles exist for some traits like blood type.
Similar to Plant Cytogenetics: Inheritance of Lethal genes. (20)
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- 1. B.SC. III: SEMESTER-VI PAPER XIX: GENETICS AND BIOTECHNOLOGY INHERITANCE OF LETHAL GENES Dr. A.S. Naik, Head, Dept. of Botany SBES College of Science
- 2. Explanation of inheritance of lethal genes. This is a deviation from Mendel’s classic onohybrid inheritance. ◦ Definition: Genes which result in viability reduction of individual or become cause of death of individuals that carry them. ◦ F2 shows genotypic ratio other than Mendel’s monohybrid ratio, as 2:1 and two phenotypic classes also in same proportion. ◦ Some examples: 1. Genes controlling chlorophyll content in leaves. 2. Coat colour in mice: Yellow, black, agouti 3. Hutington disease in humans.
- 4. Types as per time of expression.
- 7. Inheritance of lethal genes in Antirrhinum majus (Snapdragon) ◦ E. Baur (1907) observed lethal gene in Snapdragon (Antirrhinum) and found that it is characterized by variegated leaves. ◦ The “golden” variety on selfing gives rise to 2 types of offspring, golden and green in the ratio of 2:1 instead of 3: 1. ◦ The golden ones are heterozygous and the green ones breed true being recessive homozygous. ◦ The recessive allelic combination results in plants with no chlorophyll (albino) that die.
- 9. Inheritance of lethal genes in Antirrhinum • Genotype GG: Dark green leaves with adequate chlorophyll ◦ Gg: golden-green leaves (auria) ◦ Genotype-gg: White (colourless) leaves. ◦ Genotype GG breeds true-only green leaved plants ◦ If parents with aurea leaves crossed: Gg X Gg ◦ gametes of Gg: G and g ◦ Will produce F2 with changed genotypic and phenotypic ratios.
- 10. Male parent Female parent G g G GG (Green) Gg (Aurea) g Gg (Aurea) gg (albino, Lethal) Genotypic Ratio of F2: GG ¼: Gg 2/4: gg ¼ (Lethal, dies) Hence gets modified as 2:1 Phenotypic ratio: Aurea : Green-2:1 F2:
- 11. Other examples: Coat colour in mice. ◦ Example of dominant lethal genes ◦ Dominant allele in homozygous condition proves lethal.
- 12. Lethal genes in humans. ◦ Examples of human diseases caused by recessive lethal alleles include cystic fibrosis, sickle-cell anemia, and achondroplasia. Achondroplasia is an autosomal dominant bone disorder that causes dwarfism. While the inheritance of one achondroplasia allele can cause the disease, the inheritance of two recessive lethal alleles is fatal. ◦
- 13. Assignment on Lethal genes 1. In Snapdragon, Green plants are produced by gene ‘C’ that controls adequate production of chlorophyll. It is dominant over its allele ‘c’, that produces no chlorophyll and plants are albino. The homozygous condition of the ‘c’ is lethal due to total lack of chlorophyll whereas heterozygous condition ‘Cc’ produces yellow-green/Auria plants. ◦ What genotypic and phenotypic proportion can be expected from the following crosses? (a) CC X Cc (b) Cc X Cc (c) CC X cc (d) Cc X cc ◦ 2. In cattle, gene ‘A’ produces phenotypically normal legged animals and is dominant over its allele ‘a’ producing animals with amputated legs. The gene ‘A” in homozygous recessive condition-‘aa’ has a lethal effect on animals. Find out phenotypic proportion of the offspring expected from the following crosses. ◦ (a) AA X Aa (b) Aa X Aa (c) AA X aa (d) Aa X aa