More Recent Comments

Monday, August 13, 2012

Monday's Molecule #181

Last week's molecule was an intermediate in some amino acid biosynthesis pathways and the enzyme that makes it is the target of Roundup®. Replacing this enzyme with a Roundup® resistant version yields genetically modified food plants [Monday's Molecule #180].

This week's molecule is a lot more complicated. You need to identify the specific type of molecule. Defective metabolism of this molecule is associated with a famous disease. Name the disease.

Post your answers as a comment. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post mostly correct answers to avoid embarrassment. The winner will be treated to a free lunch.

There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.)

Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)

In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.

Winners will have to contact me by email to arrange a lunch date. Please try and beat the regular winners. Most of them live far away and I'll never get to take them to lunch. This makes me sad.

Comments are invisible for 24 hours. Comments are now open.

UPDATE: The molecule is ganglioside GM2. Defects in ganglioside synthesis are responsible for a number of genetic diseases in humans including Tay-Sachs disease. This is the same molecule featured in Monday's Molecule #162 back on March 19, 2012. There was no winner that time.

This week's winner is Matt McFarlane, an undergraduate. He lives in Canada but he's quite far away and probably won't make it for lunch.

Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney
Dec. 19: Joseph C. Somody
Jan. 9: Dima Klenchin
Jan. 23: David Schuller
Jan. 30: Peter Monaghan
Feb. 7: Thomas Ferraro, Charles Motraghi
Feb. 13: Joseph C. Somody
March 5: Albi Celaj
March 12: Bill Chaney, Raul A. Félix de Sousa
March 19: no winner
March 26: John Runnels, Raul A. Félix de Sousa
April 2: Sean Ridout
April 9: no winner
April 16: Raul A. Félix de Sousa
April 23: Dima Klenchin, Deena Allan
April 30: Sean Ridout
May 7: Matt McFarlane
May 14: no winner
May 21: no winner
May 29: Mike Hamilton, Dmitri Tchigvintsev
June 4: Bill Chaney, Matt McFarlane
June 18: Raul A. Félix de Sousa
June 25: Raul A. Félix de Sousa
July 2: Raul A. Félix de Sousa
July 16: Sean Ridout, William Grecia
July 23: Raul A. Félix de Sousa
July 30: Bill Chaney and Raul A. Félix de Sousa
Aug. 7: Raul A. Félix de Sousa
Aug. 13: Matt McFarlane


5 comments :

Matt said...

It is a ganglioside; a sphingosine derived glycolypid with at least one sialic acid (the sialic acid residue is shown in blue).

Tay-Sachs disease is caused by defective metablism of this molecule

Matt McFarlane
undergraduate

Nostranoodle said...

This is Mondays Molecule # 162 (March 19). GM2 ganglioside, Tay-Sachs disease

DK said...

Finally an interesting one. I am sure to be late, so a brief answer is sufficient: Tay–Sachs disease which is caused by defective hexosaminidase A. The molecule is either GM2-ganglioside or one of its derivatives.

Sean Ridout said...

This is the ganglioside GM2, and the disorder is Tay-Sachs disease.

Jean-Marc Neuhaus said...

This is ganglioside GM2, a typical sphingolipid. Tay-Sachs disease is a genetic defect preventing degradation of GM2. Its accumulation in lysosomes of neurons causes their progressive death. The disease is usually fatal during childhood.