4 ms·

Why don't we give genes names like functions? Seems like the whole thing might be easier to understand if we called a gene "butterflyStripeWidth" rathern than

by Mizza 4y ago

Why don't we give genes names like functions? Seems like the whole thing might be easier to understand if we called a gene "butterflyStripeWidth" rathern than "WntA". It's like we're writing a new core library but only using obfuscated function names.

Pigalowda 4y ago
You want Wnt to be named after butterfly stripes? Last sentence below gives away wnt and lack of it leading to colon polyps/cancer. It does a million other things though. Might as well call it signaling molecule 145626. The activation of the pathway occurs at the cellular membrane, where Wnt ligands bind to the seven transmembrane-domain protein receptors Frizzled (Fzd) and/or to the low-density lipoprotein receptor-related protein (LRP) 5/6. This interaction leads to the inhibition of the axin degradasome destruction complex, which is a multiprotein complex that controls the cytoplasmic amount of β-catenin via phosphorylation, and, thereby, triggers β-catenin degradation by the proteasome in the absence of Wnt [10]. The destruction complex comprises the tumor suppressor adenomatous polyposis coli (APC), the axin scaffold protein, and two Ser/Thr kinases: glycogen synthase kinase 3 (GSK3) β and casein kinase 1 (CK1). In the absence of Wnt ligands, CK1 phosphorylates β-catenin at Ser45 residue and GSK3β at Ser33/Ser37/Thr41 residues. Then, the β-transducin repeats-containing protein (β-TrCP), an E3-ubiquitin ligase, ubiquitinates phosphorylated β-catenin, which becomes a target for proteasomal degradation [10]. When Wnt binds to Fzd and/or LRP5/6 receptors, the Wnt/β-catenin pathway is activated and the axin degradasome is inhibited [9]. As a consequence, Dishevelled (Dvl) is activated and recruits the degradasome complex to the plasma membrane, and, thereby, promotes the interaction between LRP5/6 and axin [11,12]. Consequently, LRP5/6 is phosphorylated at specific amino acidic residues (Ser1490, Thr1530, Thr1572, Ser1590, Ser1607) [13], acting as a direct competitive inhibitor of GSK3β [14]. Moreover, inactivation of GSK3β through Akt-dependent Ser9 phosphorylation prevents the phosphorylation of β-catenin, which allows its stabilization and accumulation in the cytoplasm. Stabilized β-catenin translocates to the nucleus where it binds to transcription factors, notably T-cell factor (TCF) and lymphoid enhancing factor (LEF), TCF/LEF. This interaction displaces the co-TCF/LEF repressor Groucho, whose function under basal conditions is to compact chromatin [15]. Groucho and TCF/LEF form a multiprotein complex, which is also termed Wnt enhanceosome, that recruits transcriptional co-activators and histone modifiers such as the ATP-dependent helicase Brahma-related gene 1 (BRG1, also known as SMARCA4), cyclic adenosine mono phosphate response element (CREB)-binding protein (CBP), p300, B-cell lymphoma 9 (BCL9), and pygo [15,16]. The Wnt enhanceosome regulates chromatin remodeling and activates the transcription of β-catenin-dependent genes involved in cell growth and survival, including C-MYC, CCND1, BIRC5, and CDKN1a [9]. C-myc is a proto-oncogene that activates cyclin D1 and simultaneously inhibits p21 and p27, which leads to uncontrolled cell proliferation
- Mizza 4y ago
  The name of the gene, not the protein, but yeah you're right that butterflyStripeWidth is far too abstract. But something like, I don't know, decarboxylizeOrnithine would make a genome more "readable".
nguyenkien 4y ago
We can only guess it functions. Give concrete name like that is not very good idea
- Mizza 4y ago
  But I can't get anything at all from the name now. BRCA1 isn't descriptive at all, but suppressBreastTumor is more helpful even it's not 100% accurate. I'd rather it be our best guess description than some random letters.
  - arrosenberg 4y ago
    BRCA is an acronym for Breast Cancer, so we are already doing that to a large degree.
    - Mizza 4y ago
      A fair point, but I think that really just lends credence to what I'm suggesting, that we expand upon that, since it isn't standardized or all that useful. If you were encountering it for the first time, what would you think WntA did?
      - arrosenberg 4y ago
        I would look it up. Genes can encode for multiple things, so it doesn’t make sense to name them like variables, genetics is far far more complex than computer programs. Case in point, the Wnt gene codes for multiple developmental characteristics across insect groups - you can’t simply say they code for this wing protein, it does far more.
  - nguyenkien 4y ago
    What if we gain more knowledge, and this isn't suppressBreastTumor. What do you do now? As I see, the answer still cryptic name, and lookup table.
    - 4y ago
rolph 4y ago
we kind of do that to an extent but that confuses things. for example tumor suppressor genes, actually produce a product that, among many other things, leads to suppression of tumor activity or viability. the gene function [depending on the gene] would really be something hypothetically like -immuno signaling factor modulator gene number 9- this makes things harder to mentally catalog for a lot of people, so we use name like SONIC; KRUPPEL; HEDGEHOG; SONIC HEDGHOG. these are developmental pattern genes, and the names are subjective based on phenotype appearance, or what a researcher was doing when they observed it, etc.

by Mizza 4y ago

Pigalowda 4y ago

You want Wnt to be named after butterfly stripes? Last sentence below gives away wnt and lack of it leading to colon polyps/cancer. It does a million other things though. Might as well call it signaling molecule 145626. The activation of the pathway occurs at the cellular membrane, where Wnt ligands bind to the seven transmembrane-domain protein receptors Frizzled (Fzd) and/or to the low-density lipoprotein receptor-related protein (LRP) 5/6. This interaction leads to the inhibition of the axin degradasome destruction complex, which is a multiprotein complex that controls the cytoplasmic amount of β-catenin via phosphorylation, and, thereby, triggers β-catenin degradation by the proteasome in the absence of Wnt [10]. The destruction complex comprises the tumor suppressor adenomatous polyposis coli (APC), the axin scaffold protein, and two Ser/Thr kinases: glycogen synthase kinase 3 (GSK3) β and casein kinase 1 (CK1). In the absence of Wnt ligands, CK1 phosphorylates β-catenin at Ser45 residue and GSK3β at Ser33/Ser37/Thr41 residues. Then, the β-transducin repeats-containing protein (β-TrCP), an E3-ubiquitin ligase, ubiquitinates phosphorylated β-catenin, which becomes a target for proteasomal degradation [10]. When Wnt binds to Fzd and/or LRP5/6 receptors, the Wnt/β-catenin pathway is activated and the axin degradasome is inhibited [9]. As a consequence, Dishevelled (Dvl) is activated and recruits the degradasome complex to the plasma membrane, and, thereby, promotes the interaction between LRP5/6 and axin [11,12]. Consequently, LRP5/6 is phosphorylated at specific amino acidic residues (Ser1490, Thr1530, Thr1572, Ser1590, Ser1607) [13], acting as a direct competitive inhibitor of GSK3β [14]. Moreover, inactivation of GSK3β through Akt-dependent Ser9 phosphorylation prevents the phosphorylation of β-catenin, which allows its stabilization and accumulation in the cytoplasm. Stabilized β-catenin translocates to the nucleus where it binds to transcription factors, notably T-cell factor (TCF) and lymphoid enhancing factor (LEF), TCF/LEF. This interaction displaces the co-TCF/LEF repressor Groucho, whose function under basal conditions is to compact chromatin [15]. Groucho and TCF/LEF form a multiprotein complex, which is also termed Wnt enhanceosome, that recruits transcriptional co-activators and histone modifiers such as the ATP-dependent helicase Brahma-related gene 1 (BRG1, also known as SMARCA4), cyclic adenosine mono phosphate response element (CREB)-binding protein (CBP), p300, B-cell lymphoma 9 (BCL9), and pygo [15,16]. The Wnt enhanceosome regulates chromatin remodeling and activates the transcription of β-catenin-dependent genes involved in cell growth and survival, including C-MYC, CCND1, BIRC5, and CDKN1a [9]. C-myc is a proto-oncogene that activates cyclin D1 and simultaneously inhibits p21 and p27, which leads to uncontrolled cell proliferation

Mizza 4y ago
The name of the gene, not the protein, but yeah you're right that butterflyStripeWidth is far too abstract. But something like, I don't know, decarboxylizeOrnithine would make a genome more "readable".

nguyenkien 4y ago

We can only guess it functions. Give concrete name like that is not very good idea

Mizza 4y ago
But I can't get anything at all from the name now. BRCA1 isn't descriptive at all, but suppressBreastTumor is more helpful even it's not 100% accurate. I'd rather it be our best guess description than some random letters.
- arrosenberg 4y ago
  BRCA is an acronym for Breast Cancer, so we are already doing that to a large degree.
  - Mizza 4y ago
    A fair point, but I think that really just lends credence to what I'm suggesting, that we expand upon that, since it isn't standardized or all that useful. If you were encountering it for the first time, what would you think WntA did?
    - arrosenberg 4y ago
      I would look it up. Genes can encode for multiple things, so it doesn’t make sense to name them like variables, genetics is far far more complex than computer programs. Case in point, the Wnt gene codes for multiple developmental characteristics across insect groups - you can’t simply say they code for this wing protein, it does far more.
- nguyenkien 4y ago
  What if we gain more knowledge, and this isn't suppressBreastTumor. What do you do now? As I see, the answer still cryptic name, and lookup table.
  - 4y ago

rolph 4y ago

we kind of do that to an extent but that confuses things. for example tumor suppressor genes, actually produce a product that, among many other things, leads to suppression of tumor activity or viability. the gene function [depending on the gene] would really be something hypothetically like -immuno signaling factor modulator gene number 9- this makes things harder to mentally catalog for a lot of people, so we use name like SONIC; KRUPPEL; HEDGEHOG; SONIC HEDGHOG. these are developmental pattern genes, and the names are subjective based on phenotype appearance, or what a researcher was doing when they observed it, etc.