Iain Cheeseman
@iaincheeseman.bsky.social
Whitehead Institute and Department of Biology, MIT. Lover of cell biology and cell division. Aspiring to do good science and do good.
I got a nice gift from stellar Cheese lab graduate student Matteo Di Bernardo from his travels - who knows my love of tea. But I'm trying to figure out whether there is a message in that this tea promotes cognitive function. A little help never hurts, I guess. :-)
August 19, 2025 at 11:57 AM
I got a nice gift from stellar Cheese lab graduate student Matteo Di Bernardo from his travels - who knows my love of tea. But I'm trying to figure out whether there is a message in that this tea promotes cognitive function. A little help never hurts, I guess. :-)
The key? This happens by inhibiting deadenylation. Mitotic cells block the shortening of the polyA tail due to a stabilization of polyA binding protein (PABPC). This results in amazing "bumps" in tail length. Critically, blocking this process in mitosis results in premature mitotic exit.
July 23, 2025 at 11:03 AM
The key? This happens by inhibiting deadenylation. Mitotic cells block the shortening of the polyA tail due to a stabilization of polyA binding protein (PABPC). This results in amazing "bumps" in tail length. Critically, blocking this process in mitosis results in premature mitotic exit.
Graduate student Katya Khalizeva and team show that mRNA is robustly stabilized the moment that cells enter mitosis with >4x increase in half life. We see this for individual genes and across the transcriptome.
July 23, 2025 at 11:00 AM
Graduate student Katya Khalizeva and team show that mRNA is robustly stabilized the moment that cells enter mitosis with >4x increase in half life. We see this for individual genes and across the transcriptome.
Unexpectedly, checkpoint proteins previously considered essential—including Mad2—are not required for viability in Cdc20ΔFL cells. Our targeted functional analysis reveals that Mad2, CDK phosphorylation, and Cdc20 levels act together to define the mitotic timer - acting to buffer each other's roles.
June 16, 2025 at 11:01 AM
Unexpectedly, checkpoint proteins previously considered essential—including Mad2—are not required for viability in Cdc20ΔFL cells. Our targeted functional analysis reveals that Mad2, CDK phosphorylation, and Cdc20 levels act together to define the mitotic timer - acting to buffer each other's roles.
We leverage a unique separation-of-function allele for Cdc20 that eliminates the checkpoint activity of its full-length translational isoform. Using functional genetics, we find synthetic lethality with cell division genes and an increase in anaphase errors consistent with a surveillance role.
June 16, 2025 at 10:58 AM
We leverage a unique separation-of-function allele for Cdc20 that eliminates the checkpoint activity of its full-length translational isoform. Using functional genetics, we find synthetic lethality with cell division genes and an increase in anaphase errors consistent with a surveillance role.
I guess at least it was reviewed.
April 24, 2025 at 2:10 AM
I guess at least it was reviewed.
Beyond core cellular function, this is critical for understanding rare human disease. Alternate protein isoforms are selectively mutated in genetic disorders. You can't interpret these mutations without understanding the isoforms and they are central to the unique clinical symptoms.
March 27, 2025 at 11:53 AM
Beyond core cellular function, this is critical for understanding rare human disease. Alternate protein isoforms are selectively mutated in genetic disorders. You can't interpret these mutations without understanding the isoforms and they are central to the unique clinical symptoms.
This alternate decoding isn't just happening in human cells. It is deeply conserved with dual mitochondria and cytoplasmic variants across metazoa, fungi, and plants. However, organisms that have dispensed with aspects of mitochondrial function have lost these mitochondrial variants.
March 27, 2025 at 11:50 AM
This alternate decoding isn't just happening in human cells. It is deeply conserved with dual mitochondria and cytoplasmic variants across metazoa, fungi, and plants. However, organisms that have dispensed with aspects of mitochondrial function have lost these mitochondrial variants.
This isn't just for 1 gene. New work from @jimmy-ly.bsky.social identifies hundreds of differentially localized translational isoforms, including >100 that impact the mitochondria.
Tomorrow: We trace the ancient origins of this behavior and its impact on human disease.
Friday: Preprint drops!
Tomorrow: We trace the ancient origins of this behavior and its impact on human disease.
Friday: Preprint drops!
March 26, 2025 at 10:20 AM
This isn't just for 1 gene. New work from @jimmy-ly.bsky.social identifies hundreds of differentially localized translational isoforms, including >100 that impact the mitochondria.
Tomorrow: We trace the ancient origins of this behavior and its impact on human disease.
Friday: Preprint drops!
Tomorrow: We trace the ancient origins of this behavior and its impact on human disease.
Friday: Preprint drops!
Key activities are needed in both the mitochondria and host cell. So how do you put 1 protein in 2 places?
1) Make 2 genes w different signals, or
2) Decode a single RNA to make 2 proteins.
Our new work highlights how alternate translation initiation can create differentially localized proteins.
1) Make 2 genes w different signals, or
2) Decode a single RNA to make 2 proteins.
Our new work highlights how alternate translation initiation can create differentially localized proteins.
March 26, 2025 at 10:15 AM
Key activities are needed in both the mitochondria and host cell. So how do you put 1 protein in 2 places?
1) Make 2 genes w different signals, or
2) Decode a single RNA to make 2 proteins.
Our new work highlights how alternate translation initiation can create differentially localized proteins.
1) Make 2 genes w different signals, or
2) Decode a single RNA to make 2 proteins.
Our new work highlights how alternate translation initiation can create differentially localized proteins.
Countdown to an epic new pre-print.
Mitochondria are cells within our cells. They need the same core activities - replication, transcription, translation. How do cells enable these diverse activities in both compartments? We uncover an unexpected + broad strategy with ancient origins. Stay tuned!
Mitochondria are cells within our cells. They need the same core activities - replication, transcription, translation. How do cells enable these diverse activities in both compartments? We uncover an unexpected + broad strategy with ancient origins. Stay tuned!
March 25, 2025 at 10:35 AM
Countdown to an epic new pre-print.
Mitochondria are cells within our cells. They need the same core activities - replication, transcription, translation. How do cells enable these diverse activities in both compartments? We uncover an unexpected + broad strategy with ancient origins. Stay tuned!
Mitochondria are cells within our cells. They need the same core activities - replication, transcription, translation. How do cells enable these diverse activities in both compartments? We uncover an unexpected + broad strategy with ancient origins. Stay tuned!
ChatGPT agrees with me
February 28, 2025 at 2:05 AM
ChatGPT agrees with me
New preprint! Eric Smith and Jimmy Ly reveal a beautiful example of repurposing of a molecular machine. RNase P + RNase MRP share 9 subunits and yet are functionally very different. We find key new subunits that act as specificity factors to distinguish MRP.
www.biorxiv.org/content/10.1...
www.biorxiv.org/content/10.1...
January 29, 2025 at 11:41 AM
New preprint! Eric Smith and Jimmy Ly reveal a beautiful example of repurposing of a molecular machine. RNase P + RNase MRP share 9 subunits and yet are functionally very different. We find key new subunits that act as specificity factors to distinguish MRP.
www.biorxiv.org/content/10.1...
www.biorxiv.org/content/10.1...
My old bench. Lots of great science memories.
December 12, 2024 at 4:36 PM
My old bench. Lots of great science memories.
Getting ready to pregame @ascbiology.bsky.social with an epic reunion of the Oegema/Desai lab @odlab.bsky.social. Can’t wait to see everyone. Can’t believe it’s been 22 years since they started it all.
December 12, 2024 at 3:43 PM
Getting ready to pregame @ascbiology.bsky.social with an epic reunion of the Oegema/Desai lab @odlab.bsky.social. Can’t wait to see everyone. Can’t believe it’s been 22 years since they started it all.
New preprint! How do cells rewire chromosome segregation during meiosis? We identify a germline-specific mRNA splice isoform for a critical kinetochore protein. This alternative protein transforms its regulatory control, contributing to proper fertility.
www.biorxiv.org/content/10.1...
www.biorxiv.org/content/10.1...
April 19, 2024 at 6:37 PM
New preprint! How do cells rewire chromosome segregation during meiosis? We identify a germline-specific mRNA splice isoform for a critical kinetochore protein. This alternative protein transforms its regulatory control, contributing to proper fertility.
www.biorxiv.org/content/10.1...
www.biorxiv.org/content/10.1...
New preprint now live! We find that translation start site selection is dramatically rewired during mitosis through an elegant mechanism involving the nuclear release of eIF1. Want a play-by-play of major findings? - check out last week's teaser posts.
www.biorxiv.org/content/10.1...
www.biorxiv.org/content/10.1...
April 8, 2024 at 10:44 AM
New preprint now live! We find that translation start site selection is dramatically rewired during mitosis through an elegant mechanism involving the nuclear release of eIF1. Want a play-by-play of major findings? - check out last week's teaser posts.
www.biorxiv.org/content/10.1...
www.biorxiv.org/content/10.1...
When cells can’t release extra nuclear eIF1, start site usage doesn’t change between interphase and mitosis. This is catastrophic for cells when they experience even a modest mitotic delay with increased mitotic cell death and reduced mitotic slippage.
April 6, 2024 at 5:34 PM
When cells can’t release extra nuclear eIF1, start site usage doesn’t change between interphase and mitosis. This is catastrophic for cells when they experience even a modest mitotic delay with increased mitotic cell death and reduced mitotic slippage.
Release of a nuclear pool of eIF1 rewires translation during mitosis. But what happens if cells lack this nuclear pool? We developed a strategy to selectively eliminate nuclear eIF1 by altering the endogenous locus.
April 6, 2024 at 5:34 PM
Release of a nuclear pool of eIF1 rewires translation during mitosis. But what happens if cells lack this nuclear pool? We developed a strategy to selectively eliminate nuclear eIF1 by altering the endogenous locus.
Mitotic release of nuclear eIF1 drives the increased stringency of start codon selection. To me, this was a mind blowing mechanism to control translation allowing cells to rapidly change translation at mitotic entry and again at mitotic exit when the nucleus reforms.
April 6, 2024 at 5:31 PM
Mitotic release of nuclear eIF1 drives the increased stringency of start codon selection. To me, this was a mind blowing mechanism to control translation allowing cells to rapidly change translation at mitotic entry and again at mitotic exit when the nucleus reforms.
Most translation factors are in the cytoplasm. Instead, eIF1 localizes to both the cytoplasm AND the nucleus. This nuclear pool of eIF1 can’t interact with ribosomes, but mitotic nuclear envelope breakdown releases this extra eIF1.
April 6, 2024 at 5:30 PM
Most translation factors are in the cytoplasm. Instead, eIF1 localizes to both the cytoplasm AND the nucleus. This nuclear pool of eIF1 can’t interact with ribosomes, but mitotic nuclear envelope breakdown releases this extra eIF1.
We found that the translation stringency factors eIF1 and eIF5 show differential associations with the 40S during mitosis. Increased eIF1 levels are known to ensure that only the most efficient start sites are used – a molecular explanation for our mitotic translation rewiring.
April 5, 2024 at 10:48 AM
We found that the translation stringency factors eIF1 and eIF5 show differential associations with the 40S during mitosis. Increased eIF1 levels are known to ensure that only the most efficient start sites are used – a molecular explanation for our mitotic translation rewiring.
How is translation start site usage dramatically rewired in mitosis? The key is the start codon. In interphase, both AUG and non-canonical start sites (i.e., CUG) are well used. In mitosis, only the “best” start sites are used - non-canonical sites are preferentially repressed.
April 3, 2024 at 4:14 PM
How is translation start site usage dramatically rewired in mitosis? The key is the start codon. In interphase, both AUG and non-canonical start sites (i.e., CUG) are well used. In mitosis, only the “best” start sites are used - non-canonical sites are preferentially repressed.
We mapped >15,000 translation start sites using ribosome profiling. What blew our minds is that relative start site usage was transformed in mitosis, going both up and down. This affects 1000s of canonical proteins, alternative isoforms, and uORFs.
April 3, 2024 at 4:13 PM
We mapped >15,000 translation start sites using ribosome profiling. What blew our minds is that relative start site usage was transformed in mitosis, going both up and down. This affects 1000s of canonical proteins, alternative isoforms, and uORFs.