Revisitando a história da genética clássica: dos caracteres unitários ao gene (1900-1926)

O presente artigo se refere ao período da chamada genética clássica. Seu objetivo é discutir sobre as concepções e terminologia aplicadas ao material hereditário entre 1900 (“redescoberta” do trabalho de Mendel) e a publicação do livro The theory of the gene (1926) de Thomas Hunt Morgan (1866-1945), procurando averiguar se houve mudanças em relação a esses aspectos durante o período. O foco de nossa análise são as contribuições de dois grupos: o grupo britânico liderado por William Bateson (1861-1926) e o grupo norte-americano, liderado por Morgan. No período estudado, a terminologia foi mudando de “fator”, “caracteres”, “caracteres-unitários” e “gene”, que foi adotado a partir de 1926. Apesar de Bateson e Morgan considerarem que os agentes hereditários estivessem nas células germinativas, desconheciam sua composição. Esta pesquisa mostrou que durante o estabelecimento de uma nova área de estudo vão ocorrendo modificações em relação à terminologia empregada bem como à conotação dos termos, até que haja um consenso por parte da comunidade científica que os adote.

The Matilda Effect

This chapter suggests that the most important factors that diminished Esther Lederberg’s scientific career and legacy were her gender and marriage. The fact that her famous collaborator was also her husband doubled the chances that her own scientific achievements were overshadowed. The chapter goes on to explain how the so-called Matthew and Matilda Effects altered the history of science right at birth of genetics as a distinct branch of biology. As an example of the Matilda Effect, the chapter presents Nettie Stevens whose discovery of the XY sex-determining chromosomes in 1905 and establishment of the two patterns of sex chromosomes in various beetles, flies, and bugs was credited to Edmund Wilson, a better-known scientist. In an example of the Matthew Effect, Thomas Hunt Morgan, the most famous geneticist of the early twentieth century, eventually received most of the credit for discovering sex chromosomes. Finally, the careers and legacies of three other Matildas who worked in the early days of microbial genetics—Martha Chase, Laura Garnjobst, and Daisy Dussoix—are presented.

Gregor Mendel, Thomas Hunt Morgan en experimenten in de klassieke genetica

Gregor Mendel, Thomas Hunt Morgan and experiments in classical geneticsIn the middle of the 19th century, Gregor Mendel performed a series of crosses with pea plants to investigate how hybrids are formed. Decades later, Thomas Hunt Morgan finalized the theory of classical genetics. An important aspect of Mendel’s and Morgan’s scientific approach is that they worked in a systematic, experimental fashion. But how did these experiments proceed? What is the relation between these experiments and Mendel’s and Morgan’s explanatory theories? What was their evidential value? Using present-day insights in the nature of experimentation I will show that the answer to these questions is fascinating but not obvious. Crossings in classical genetics lacked a crucial feature of traditional experiments for causal discovery: manipulation of the purported causes. Hence they were not traditional, ‘manipulative’ experiments, but ‘selective experiments’.

“…this Brazilian venture…” A brief biography of Theodosius Dobzhansky before he arrived in Brazil

This paper describes life and career of Theodosius Dobzhansky (1900-1975) until he arrived in Brazil in 1943. During his years in Russia, Dobzhansky began his entomology studies and undertook research expeditions to Central Asia to study livestock, which focused on speciation biology. Once he arrived in the United States Dobzhansky began working with Drosophila melanogaster with Thomas Hunt Morgan (1866-1945) at Columbia University. Once Morgan relocated to the California Institute of Technology (Caltech), Dobzhansky started collaborating with his colleague, Alfred Henry Sturtevant (1891-1970), on studies of a wild cousin of Drosophila melanogaster, Drosophila pseudoobscura. Dobzhansky and Sturtevant’s friendship and collaboration suffered due to several factors, including most importantly, their differing approaches to Drosophila pseudoobscura as influenced by their different conceptions of the purpose of their work. While Sturtevant studied the flies using the same techniques as his studies of the domestic Drosophila melanogaster, Dobzhansky studied Drosophila pseudoobscura in the field considering his broader dictum that “Nothing in biology makes sense except in the light of evolution.”

A Morgan Legacy

The Thomas Hunt Morgan Medal recognizes lifetime contributions to the field of genetics. The 2020 recipient is Gerald R. Fink of Massachusetts Institute of Technology and the Whitehead Institute for Biomedical Research, recognizing the discovery of principles central to genome organization and regulation in eukaryotic cells.

Perspective: Linkage Maps, Communities of Geneticists, and Genome Databases

The Thomas Hunt Morgan Medal recognizes lifetime contributions to the field of genetics. The 2020 recipient is David Botstein of Calico Labs and Princeton University, recognizing his multiple contributions to genetics, including the collaborative development of methods for defining genetic pathways, mapping genomes, and analyzing gene expression.

speck, First Identified in Drosophila melanogaster in 1910, Is Encoded by the Arylalkalamine N-Acetyltransferase (AANAT1) Gene

The pigmentation mutation speck is a commonly used recombination marker characterized by a darkly pigmented region at the wing hinge. Identified in 1910 by Thomas Hunt Morgan, speck was characterized by Sturtevant as the most “workable” mutant in the rightmost region of the second chromosome and eventually localized to 2-107.0 and 60C1-2. Though the first speck mutation was isolated over 110 years ago, speck is still not associated with any gene. Here, as part of an undergraduate-led research effort, we show that speck is encoded by the Arylalkylamine N-acetyltransferase 1 (AANAT1) gene. Both alleles from the Morgan lab contain a retrotransposon in exon 1 of the RB transcript of the AANAT1 gene. We have also identified a new insertion allele and generated multiple deletion alleles in AANAT1 that all give a strong speck phenotype. In addition, expression of AANAT1 RNAi constructs either ubiquitously or in the dorsal portion of the developing wing generates a similar speck phenotype. We find that speck alleles have additional phenotypes, including ectopic pigmentation in the posterior pupal case, leg joints, cuticular sutures and overall body color. We propose that the acetylated dopamine generated by AANAT1 decreases the dopamine pool available for melanin production. When AANAT1 function is decreased, the excess dopamine enters the melanin pathway to generate the speck phenotype.

speck, first identified in Drosophila melanogaster in 1910, is encoded by the Arylalkalamine N-acetyltransferase (AANAT1) gene

The pigmentation mutation speck is a commonly used recombination marker characterized by a darkly pigmented region at the wing hinge. Identified in 1910 by Thomas Hunt Morgan, speck was characterized by Sturtevant as the most 'workable' mutant in the rightmost region of the second chromosome and eventually localized to 2-107.0 and 60C1-2. Though the first speck mutation was isolated over 115 years ago, speck is still not associated with any gene. Here, as part of an undergraduate-led research effort, we show that speck is encoded by the Arylalkylamine N-acetyltransferase 1 (AANAT1) gene. Both alleles from the Morgan lab contain a retrotransposon in exon 1 of the RB transcript of the AANAT1 gene. We have also identified a new insertion allele and generated multiple deletion alleles in AANAT1 that all give a strong speck phenotype. In addition, expression of AANAT1 RNAi constructs either ubiquitously or in the dorsal portion of the developing wing generates a similar speck phenotype. We find that speck alleles have additional phenotypes, including ectopic pigmentation in the posterior pupal case, leg joints, cuticular sutures and overall body color. We propose that the acetylated dopamine generated by AANAT1 decreases the dopamine pool available for melanin production. When AANAT1 function is decreased, the excess dopamine enters the melanin pathway to generate the speck phenotype.